Specialist Answers on Kidney Disease

Q1. My grandmother was recently put on dialysis. They say this may prevent her from urinating normally. Is this true? What should we expect?

— Chrissy, Michigan

Dialysis, a procedure that uses a special machine to replace the kidneys in filtering waste from the bloodstream, may reduce the daily urine output that a person normally produces. This happens because as the blood is filtered during dialysis, fluid is removed, thus reducing the kidneys’ traditional role. As a result many dialysis patients produce very small amounts of urine. However, dialysis does not prevent someone from urinating normally; it only reduces the total urine output, so that he or she may only need to urinate once a day, which is not dangerous. Some dialysis patients produce as little as one cup or less of urine each day, though urine volume is usually dependent on the underlying cause of kidney failure. Some patients continue to produce normal volumes of urine, which helps to manage their fluid balance. You should be able to get more information from your grandmother’s doctor, a nephrologist. This medical specialist is experienced in treating kidney disease and can provide insight into the cause of your grandmother’s kidney failure.

Q2. My husband was told that he has cysts in his kidneys. The doctor doesn’t seem concerned, but my husband says that when he urinates, he sometimes feels as if he is being kicked in the back. He also has an enlarged prostate, so he urinates frequently. He had a prostate biopsy last year that showed no cancer, but his PSA level is elevated. What causes these kidney cysts, and are they in any way related to the prostate problem?

Most kidney cysts are completely benign and, once recognized by either ultrasound or CT imaging, do not need additional follow-up. Some kidney cysts have genetic causes, but they have a characteristic pattern, occur in particular age groups, and are very rare. Benign cysts have well-established characteristics: an imperceptibly thin wall, no interior debris, and a clear fluid inside that has the same density as water. More complex cysts feature thicker walls and internal echoes, where areas of calcification, or hardened tissue, need further significant follow-up. Your husband’s urinary symptoms may be consistent with his age. Back pain associated with urination, on the other hand, is an uncommon condition. It may be related to the reflux of urine from the bladder to the kidney and would usually be associated with other abnormalities seen on X-ray.

Kidney cysts develop as a result of the thinning and expansion of some of the tubular structures of the kidney. They are not related to prostate problems and occur with the same frequency in men and women.

Q3. I have medullary sponge kidney disease and have passed stones of all sorts of colors, shapes, and sizes. Are there really different types of kidney stones, and if so, is the type I’m experiencing now (white in color) of any greater concern?

— Kimberly, Kentucky

Kidney stones do come in all sorts of colors. Many are white, but others are black, or come in various shades of color. Medullary sponge kidney disease can be associated with the formation of calcium oxalate stones, which come in a variety of shapes and sizes. More important than the color, however, is the composition of the stone, which can include calcium oxalate, calcium phosphate, and a number of other compounds.

Treatments to prevent a recurrence of these stones will focus on the type of stone you have, its composition, and any underlying metabolic disorders that may predispose you to the formation of stones. For this reason, it’s important to involve a medical or surgical specialist in your care. Together, you can develop a long-term strategy for managing your medullary sponge kidney disease and for preventing recurrent kidney stone formation.

Learn more about disease prevention in the Everyday Health Healthy Living Center.

Explained: The Value of Residual Kidney Function to Dialysis

A home haemodialysis patient from New Zealand asked the Home Dialysis Central Facebook discussion group: “Why do dialysis patients have different outcomes with regard to maintaining residual kidney function?” And, “Why do some people seem to have an easier time than others with the control of salts like sodium, potassium, and phosphate?”

My first response must be that while the functions of the normal kidney are well known, the myriad variable and interrelating dysfunctions of kidney physiology (or, functional pathophysiology) that occur once dialysis begins, are not. Indeed, I almost despaired of making any sensible contribution as few (if any) studies have looked at the contribution residual renal function makes (if any) to electrolyte regulation in dialysis patients!

But, home patients (especially) are an inquisitive lot. They often ask interesting questions as they seek to understand the unknown. So, for them, I resolved to give it my best shot. My answer has grown into a gargantuan beast, but, here goes…

Residual Renal Function (RRF)

RRF is a term often used to describe the remaining contribution, or contributions—note the plural—the last remnants of failing kidney tissue may still make to overall water and waste clearance, once dialysis has begun.

It can seem contradictory to patients, especially home patients who are struggling to understand the therapy they are self-applying, that despite being told they need dialysis, they may still be passing what seems like plentiful urine. On the other hand, some do not pass much urine. Why the difference?

RRF – to patients – can mean different things. Some interpret it to predominantly signify preserved (or lost) urine output. Others think of it in terms of clearance of wastes. Still others, a combination of the two. In truth, all are correct, depending on the circumstance.

How Kidneys Work

Our kidneys make urine, which provides our physiology (normal body function) with two basic things:

1. A balance and control of the exact amount of water and right concentration of the salts (electrolytes) that fill and bathe our cells, structures and organs. Electrolytes are simply chemicals that, when dissolved in water, are positively or negatively charged (like a battery) and can transmit electricity. Common electrolytes include sodium, chloride, potassium, calcium, phosphate, magnesium, bicarbonate, and many others. By losing or retaining water, and by excreting or reclaiming electrolytes, the kidneys finely regulate and adjust the volume of water and the concentration of salts in body tissues.
2. They filter away (or “clear”) all the waste substances that our cells, structures and organs make in their daily functioning. This is why the term “clearance” is used for the excretory function of the kidneys.

To perform these two functions—water and electrolyte balance, and waste clearance—the kidneys have evolved an exquisite mechanism: the nephron.

Each kidney contains an average of about one million nephrons, though the range between individuals and racial origins is very wide. For example, Australian aboriginals tend to be nephron poor, having as few as 350,000 nephrons per kidney, while some Caucasians may have as many as 1.5 million per kidney.

Low nephron number has many possible causes, some of which appear genetically determined, but nephron number may be key to the ability to withstand or cope with kidney disease. It may be one of the underlying reasons why some people (perhaps with a higher nephron number) seem more resilient to the same “hit” of the same disease than others (who perhaps have a lower nephron number). One day, when we can accurately count nephrons, we may have a tool to aid in outcome prediction…but this is not yet practically possible (except at autopsy!).

Different Parts of Kidneys Do Different Tasks

Each human nephron has two distinct parts:

1. A glomerulus (a leaky filter)

2. A tubule (a filtrate modifier)

Simplistically, glomeruli (= the plural of glomerulus) filter solutes (electrolytes + wastes) and water out of the bloodstream as blood passes through the kidneys. They “sweat” a fluid and solute mix across their leaky membrane walls—a bit like those leaky black garden hoses do.

Staggeringly though, more than 180 liters of water and solutes “sweat” across the glomerular membrane and into the tubules every 24 hours. That is a fluid volume equal in weight to about 2 ½ times the body weight of an average human! Clearly, we would not live more than a few minutes if that enormous amount of fluid were to pass, unaltered, as our final urine. Something magical must happen to it as it passes through the tubular system – allowing the body to grab back most of the water and salts, but allowing continued waste excretion.

The tubules must reabsorb almost all the fluid that poured through the glomeruli, and leave a mere 1.5 – 2.0 liters to be passed as the final fluid we call urine. But, that urine must still contain all the solute wastes that must be eliminated. The renal tubule—one for each glomerulus—is a very smart and complicated structure!

The tubules are a frantic two-way interface. While some things are being reclaimed from the tubular fluid, others are being exchanged and/or excreted. Think of a post office: letters and parcels of all shapes and sizes in, letters and parcels of all shapes and sizes out.

The renal tubule is a hive of industry. Tubules suck back (reabsorb) all but 1.5 – 2.0 of the 180+ liters that are unselectively washed through the glomerulus each 24 hours:

• Most of the filtered sodium is returned to the bloodstream.

• Potassium, calcium, magnesium, bicarbonate, glucose and most proteins are reabsorbed.

• Additional creatinine and uric acid (urate) is excreted.

• Urea is reabsorbed to help reclaim water.

While the glomeruli provide a non-selective waterfall of fluid and solutes, the tubules adjust this torrent to ensure that the final urine is volume and content perfect. Water, glucose, and electrolytes are balanced for physiological need—but the urine is waste-rich to ensure that as much waste is eliminated as possible.

There are, broadly, four different sections in each renal tubule—with each section performing a different set of tasks. Tubular function is regulated by a raft of osmotically-active hormones: anti-diuretic hormone (also known as vasopressin), natriuretic hormone, aldosterone, and others. Lots of energy-requiring chemical pumps inhabit the cells that line the tubules, reading, adjusting, pumping and transporting substances into and out of the tubular fluid to ensure the internal chemistry of the blood is kept “just so. ”

Again, renal tubules are very complicated structures!

Why Are There Different Responses to Kidney Disease?

When kidney diseases strike, nephrons can be damaged in different ways and at different sites along their length. This depends on the disease process (there are scores of kidney diseases), and on the part (or parts) of the nephron that are damaged by each disease:

• Some diseases predominantly damage the glomerulus.

• Others may cause more damage to tubular cells and structures.

• Many do both—with varying degrees of scarring and fibrosis (a gristly thickening of the cellular tissues) affecting glomeruli, tubules, and the interstitium of the kidney—the part that occupies the space between nephrons, supporting them, and providing a two-way pathway between the tubules and the microcirculation of the kidney.

But, when one part of the nephron is damaged, it affects other parts, too, even if those are spared direct damage. And, as nephrons are damaged, their function is compromised, altered, or completely lost.

Damage can occur at different rates, too. Tubular damage may occur at different parts of each tubule, and thus affect different functions differently. And, to make it even harder, damage and cellular death can be very patchy, with some parts of the kidney being relatively spared while other parts are being damaged beyond recognition. So, even the same disease can damage different people in different ways.

Why Does CKD4 Eventually Progress to Dialysis?

I use this example with my patients:

Imagine a factory making a product: any factory, any product. It employs 100 workers. The bean-counters come in and make 50 workers (50% of the work force) redundant. The other 50 would work some overtime, grumble now and then, but still keep the factory running and producing its product, even if it means working a little harder.

But, then they fire another ½ of the work force. Now, the factory is down to only 1 in 4 of its original staffing. A point is reached where—even with all the goodwill in the world, with all the harder work—the product just cannot be made. The factory output begins to fall, and it is no longer profitable. Its workers begin to get sick, just from overwork, and leave. Still more may choose to leave. As more and more fall ill, or leave, the strain on those remaining gets more, and more. The factory is no longer sustainable. It closes down.

This is just how it is with kidney function and kidney failure. Lose half, and the other half will cope. But, lose 3/4, and there is not enough left to sustain long-term function. While some more may be lost by disease, other still-functioning nephrons begin to “pack it in” from overwork. A point of self-fulfilling failure has been reached. Kidney failure becomes inevitable.

Back to Residual Renal Function

RRF – more particularly, residual urine output—matters, for several reasons:

1. In peritoneal dialysis patients, where solute clearance is not quite as efficient as that which is normally provided by haemodialysis, even severely damaged kidneys can still contribute important—even if small—additional solute removal.

2. In both modalities—though, this time, more importantly in haemodialysis—a sustained urine output means a freer, more comfortable fluid intake, and easier fluid management. Clearly, if urine output can be preserved, then both the ultrafiltration volume and the rate of ultrafiltration (fluid removal) can be—must be—correspondingly reduced. While ultrafiltration does increase solute drag and thus solute removal, this effect is not necessary for solute removal…it simply enhances it—but only to a small extent.

3. But…the home haemodialysis patient who maintains a good urine output is in an enviable position. At home, sessional length can be easily extended. The clearance gained from a longer session more than makes up for any (small) loss of clearance that may result from a lower or isovolaemic (= no change in net volume) ultrafiltration (UF) rate. Fluid management can be kept far more comfortable. I have read that some home patients are being told they must ultrafilter a stipulated minimum amount. But, if their urine output is sustained, their interdialytic weight gain is small, and their blood pressures are normal, their UF rate can and should be adjusted downwards, relative to sessional length, and the amount of fluid that needs removal to return to target weight. They ought not be illogically forced to maintain some arbitrary “prescribed rate.” The whole point of home haemodialysis dialysis is the immeasurable advantage that a patient can gain from lengthening the session. A longer session permits a lower rate of fluid removal, to the lasting benefits of both well-being and survival.

4. A low UF rate reduces or even completely negates any contraction of the blood volume (= isovolaemic dialysis). A stable blood volume will ensure that the blood pressure will remain stable and hypotension will be prevented.

5. Preventing in-treatment hypotension will ensure that organ perfusion will be sustained throughout the dialysis session: not only sustaining myocardial perfusion (a happier heart), cerebral perfusion (a less fogged brain), and gut perfusion (a less grumbly tummy), but will ensure preserved perfusion of the residual kidneys. This will ensure that urine output is not “turned off’ by the repeated and aggressive blood volume contraction that accompanies high ultrafiltration rate dialysis.

6. And so, the circle is completed. A sustained urine volume is preserved. Easy ongoing fluid management results, and residual renal function is sustained.

While this does not fully answer all of the questions the patient asked—for there really are no certain answers to all his questions—it does explain why any dialysis prescription that can lower the hourly UF rate is beneficial.

The data tells us that the lower the UF rate, the better: provided that a compensatory increase in session time is also prescribed to counterbalance any (small) loss of UF-driven clearance. It is all about long, slow, and gentle. Short, fast, and hard is just not correct. And…the sooner we learn this lesson, the better.

Does Changing the Volume Matter? The Relationship of Urine Volume and Dialysis Intensity

Despite many recent studies focused on novel biomarkers, urine volume remains one of the most important factors associated with renal prognosis. In patients with ESRD on either peritoneal dialysis or hemodialysis, urine output is often considered a marker of residual renal function, and preservation of residual renal function has shown contribute significantly to the overall health of patients on RRT (1–4). Along the same lines, AKI is typically defined by either increases in serum creatinine or decreases in urine output (5), and nonoliguric AKI is well known to be associated with better prognosis than oliguric AKI (6–8). However, it does not seem that the use of diuretics to convert oliguric (≤400 ml urine output daily) to nonoliguric AKI affects patient outcomes (9–11), and the clinical use of diuretics in patients with AKI remains controversial (12–14).

In fact, at present, our only therapy for severe AKI is supportive care, including RRT. Consequently, there has been significant interest in the optimal provision of RRT, including the timing, modality, and intensity of therapy. The Veterans Affairs (VA)/National Institutes of Health Acute Renal Failure Trials Network (ATN) Study and the Australian and New Zealand Intensive Care Society Randomized Evaluation of Normal Versus Augmented Level (RENAL) Study were large randomized clinical trials that evaluated the potential benefit of higher intensity RRT (15,16). The ATN Study enrolled 1124 patients at 27 VA and university–affiliated medical centers across the United States; patients were randomly assigned to receive either more intensive RRT (hemodialysis/sustained low–efficiency dialysis six times per week or continuous venovenous hemodiafiltration [CVVHDF] at 35 ml/kg per hour, with selection of modality on the basis of hemodynamic stability) or less intensive RRT (hemodialysis/sustained low–efficiency dialysis three times per week or CVVHDF at 20 ml/kg per hour). The RENAL Study randomized 1508 patients in Australia and New Zealand to receive CVVHDF at a dose of 40 or 25 ml/kg per hour. Both studies showed that more intensive RRT did not have any beneficial effects on mortality, renal recovery, or nonrenal organ failure compared with less intensive RRT. Subsequently, there has been a tremendous interest in the potentially deleterious effects of higher intensity dialysis, including the potential effect on antibiotic levels and the increased incidence of intradialytic hypotension reported in the ATN Study in the more intensive therapy arm (a similar effect was not observed in the RENAL Study, likely because patients received almost exclusively CVVHDF).

Given the prior studies suggesting a potential relationship between lower urine volumes and adverse outcomes, McCausland et al. (17) sought to explore the relationship of more intensive RRT with urine volume in the ATN Study. They hypothesized that more intensive RRT would be associated with lower urine volumes (17). To avoid the competing risk of death, they focused on only those patients who survived to day 7 (n=871) (17). In line with the original study findings, there were no differences in the baseline characteristics of the two treatment arms in this subgroup.

In the primary analysis, linear regression models were used to evaluate the effect of RRT intensity on change in urine output over the first 7 study days. In the unadjusted analysis, urine output increased by 23.2 ml/d with less intensive RRT and decreased by 8.5 ml/d with more intensive RRT, resulting in an overall difference of 31.7 ml/d. Similar trends were observed in subsequent analyses that adjusted for sex, age, race, oliguria, weight, height, heart disease, congestive heart failure, peripheral vascular disease, hypertension, stroke, liver disease, diabetes, malignancy, and the cardiovascular component of the Sequential Organ Failure Score (SOFA) score. Interestingly, a much smaller effect was observed when the same analysis was restricted to those who survived to day 28.

There was no evidence of effect modification by RRT modality but marginal evidence for effect modification by baseline urine output. Consequently, in an analysis stratified by baseline urine output, those who were oliguric (defined as the 25th percentile of urine output; 110 ml) and randomized to the lower intensity RRT arm had a more modest increase in urine volume compared with those who were nonoliguric and randomized to the lower intensity RRT arm (11.4 ml/d; 95% confidence interval [95% CI], −17.0 to 39.8 versus 45.7 ml/d; 95% CI, 14.2 to 77.2).

For the secondary analysis, Cox proportional hazards analysis was used to evaluate the time to decline in urine output by ≥50% to day 28. More intensive RRT was associated with an increased risk of a decline in urine output by ≥50% (hazard ratio, 1.29; 95% CI, 1.10 to 1.51; P=0.001). However, similar to the findings in the primary study, there was no difference in the rate of dialysis dependence to day 28 or 60 in this subcohort of survivors, and therefore, these changes in urine output with more intensive therapy could not be associated with poorer long–term outcomes. This is not incongruous with prior studies that have reported an increased risk of death in those with lower urine output, because all of these analyses were conducted after initiation of RRT, whereas many of the prior studies have examined urine output immediately before RRT initiation (6–8).

McCausland et al. (17) also conducted a number of analyses to examine factors that might mediate the relationship between more intensive RRT and lower urine output, including time–dependent SOFA score (as a measure of hemodynamic instability), BUN (as a measure of osmotic load), and overall fluid balance. However, by virtue of the treatment itself, time–dependent SOFA score may have been higher (because of more episodes of hypotension) and BUN was lower (by design) in the more intensive RRT arm; consequently, one might expect these factors to attenuate the association between more intensive RRT and urine volume, regardless of causality, and inferences about causality are difficult to make. In the case of fluid balance, fluid balance was, in fact, more negative in the less intensive RRT arm, suggesting that fluid overload was not responsible for the association of less intensive RRT with higher urine volume.

Although this is a well executed study, we believe that some caution needs to be applied to the statement that the findings of this study are “consistent with a potentially early adverse effect of more intensive RRT on residual renal function” (17). There is no doubt that urine output is lower in those receiving more intensive RRT, and there is no doubt that clinicians often use urine output as a surrogate for early renal recovery. In fact, even in the ATN Study, urine output of >30 ml/h (720 ml/d) was one of the clinical criteria used to identify patients who might have renal recovery; these patients subsequently underwent a timed creatinine clearance to assess renal function (15). However, in this subgroup analysis of the ATN Study by McCausland et al. (17), there were no reported differences in rates of dialysis dependence and presumably, no difference in time to renal recovery (although these data were not shown). Thus, it is not clear that the lower urine output observed here associates with less residual renal function. However, one of the other deleterious effects of more intensive RRT is presumably a failure to recognize and assess patients who may be in early renal recovery. For example, Figure 1 in the work by McCausland et al. (17) illustrates that, after day 1, more patients in the more intensive arm would meet the conventional definition of oliguria (e.g., urine output <400 ml/d). Because recognition of early renal recovery often hinges on the dichotomy of conventional oliguria/nonoliguria, it is possible that clinicians might view patients in the less and more intensive arms differently on the basis of residual urine output.

This study also highlights the potential importance of secondary data analyses from large randomized clinical trials. Such post hoc analyses are an excellent economic, ethical, and resourceful way to conduct hypothesis-generating studies using robust and well organized data (in this case, creating a unique opportunity to test the effect of RRT intensity on changes in urine output, while minimizing the effect of confounding by the original randomized study design). The reader must (as McCausland et al. [17] highlight throughout) keep in mind that the initial study was designed to examine other outcomes as well as the selection and survivor bias that arise in subgroup analyses that only include study survivors to days 7 and 28. This is a major potential challenge of all studies of critically ill patients where mortality is high.

In sum, McCausland et al. (17) show yet another way in which more intensive RRT is not beneficial and may even be harmful: through a decline in urine output. Although this analysis does not show an association with longer-term outcomes, including dialysis dependence at day 28 or 60, there certainly seems to be no benefit with more intensive dialysis. With regards to recognition of renal recovery, there may be delay with the more intensive arm as well. It does not seem that this association is mediated by volume overload, because volume status was actually more negative in the less intensive arm—therefore, one cannot conclude that patients receiving less intensive therapy were more volume overloaded and consequently, had greater urine output. At present, the optimal volume status to allow for renal recovery is unknown and an area of great clinical interest. Consequently, in addition to studies to define other important characteristics of RRT for patients with AKI (such as timing of initiation), future studies should focus on optimal volume management for patient receiving RRT to reduce mortality and enhance renal recovery.

Disclosures

K.D.L. has no disclosures relevant to this editorial. She has consultancy agreements with Achaogen, Astute, Durect, Genentech, ZS Pharma, and Cheetah and holds stock in Amgen.

Acknowledgments

C.K.F. is funded by the Lundbeck Foundation Clinical Research Fellowship Program.

Footnotes

• Published online ahead of print. Publication date available at www.cjasn.org.

• See related article, “Comparison of Urine Output among Patients Treated with More Intensive Versus Less Intensive RRT: Results from the Acute Renal Failure Trial Network Study,” on pages 1335–1342.

• Copyright © 2016 by the American Society of Nephrology

Case Report and Registry Data

Objective. Uncertainty has arisen as to whether renal function can be recovered from after long-term regular dialysis treatment. We therefore conducted an analysis and scrutinized one patient report. Material and Methods. Swedish registry of patients with kidney disease and one patient case. Results. 39 patients (0.2%) from the Swedish registry comprising 17590 patients who commenced RRT (renal replacement therapy) between 1991 and 2008 had recovered from renal function after more than 365 days of regular dialysis treatment. The most common diagnosis was renovascular disease with hypertension but a large group had uremia of unknown cause. HUS, cortical/tubular necrosis, and autoimmune diseases were also found. The mean treatment time before withdrawal was 2 years. Conclusions. A small number of patients recover after a long period of regular dialysis treatment. One could discuss whether it is difficult to identify patients who have recovered while undergoing regular dialysis treatment. Regular monitoring of renal function may be important.

1. Introduction

Recovery of renal function in end-stage renal disease in patients receiving renal replacement therapy has been described as occurring in 0.3%–8% [1–3]. A recent study from Australia revealed that recovery occurred in 1% of the dialysis population and there was no difference between PD or HD [4]. In the literature the cases of recovery have included various diagnoses: surgery after total renal artery arteriosclerosis, cholesterol crystal embolism, FSGS secondary to HIV, secondary oxalosis, and accelerated hypertension.

Having experienced a patient who was taken off from dialysis treatment after 15 months and who 18 months after this process is still in no need of regular dialysis motivated us to present the case and scrutinize the Swedish registry to find similar cases with dialysis treatment of more than one year followed by withdrawal. We considered it important to establish the diagnoses behind the diseases that could abate after such a long treatment period.

2. Results

We present our case report.

2.1. Case Report

A healthy 49-year-old man developed acute problems with headache and vomiting. He was admitted to hospital in November 2006. It was found that his blood pressure was high measuring 228/138 mm Hg in the left arm and 205/145 in the right arm, kidney function poor with creatinine 997 mol/L, anemia with Hb 90 g/L, and thrombocytopenia with platelets . Further investigation revealed that lactate dehydrogenase (LD) was elevated to 38.2 cat/L ( cat/L) and aspartaminotranspheras (ASAT) to 1.67 cat/L ( cat/L). The peripheral blood smear showed schistocytes and spherocytes and several reticulocytes. The clinical diagnosis was HUS and plasmapheresis was administered. The substitution fluid was plasma. However, the patient did not tolerate the treatment and became anuric with pulmonary edema. His creatinine level had now risen to 1247 mol/L. Hemodialysis was started acutely on the 12th of November and after that provided regularly three times per week. On the 23rd of November a kidney biopsy was performed. It showed severe vascular changes and several collapsed glomeruli compatible with the diagnosis of thrombotic microangiopathy and malignant hypertension. Immunofluorescence was negative.

The dialysis treatment continued and blood pressure treatment included 4 drugs (enalapril, candesartan, felodipine and metoprolol). The diuresis started to reappear and in January 2007 it was measured to 1700 mL between two dialysis schedules. He had received a central dialysis catheter on the 15th of November and an AV fistula was created in the end of January which however thrombotized. The size of the kidneys was not measured at this time point. In February 2007 an AV fistula was constructed in the upper arm, which worked perfectly and still is functioning well.

In May 2007 kidney transplantation was discussed and his sister was investigated as a donor. However, it turned out that she had had several DVTs and was thus deemed unsuitable for donation. The coagulation investigation of our patient indicated that he was heterozygote for APC resistance. The patient told us that he had good diuresis and therefore a measurement of kidney function was performed. A 48-hour iohexol clearance measurement showed a value of 9.7 mL/min/1.73 m² body surface. The transplantation plans were changed. The dialysis schedule was instead reduced to twice per week. The patient’s blood pressure was stable and well controlled by the four drugs and diuretics (Table 1).

Time Nov. 2006 May 2007 Jan. 2008 Mar. 2008 May 2008 Sep. 2008 Feb. 2009 Mar. 2009 June 2009 Oct. 2009 s-crea mol/L 397 367 406 509 386 278 309 212 s-urea mmol/L 34.4 33.4 40.5 21.2 25 Cystatin C-based eGFR mL/min/1.73 m2 body surface 24 16 17 21 20 24 Iohexol Clearance mL/min/1. 73 m2 body surface 9.7 13 16 21 23 Hemodialysis X Start X From 3 to 2 times/week X From 2 to 1 time/week Stop X 3 acute sessions X 1 acute session

In September 2007 it became possible to withdraw the EPO treatment due to a stable hemoglobin value of around 129 g/L.

In January 2008 a new 48-hour iohexolclearance measurement yielded a value of 13 mL/min/1.73 m² body surface. The dialysis treatment was further reduced to once a week.

On the 13th of March, which was 514 days after the start of renal replacement, the dialysis treatment was withdrawn completely. The patient was monitored every week. He felt very well. In May 2008 the iohexol clearance was 16 mL/min/1.73 m² body surface. The time between checkups was now extended to 2-3 weeks. S-creatinine varied between 320 and 410 mol/L.

In August the patient went to Thailand for a 4-week vacation. When he returned he was hypotonic and acidotic with uremic signs. His s-creatinine was 509 and urea was 33.4. After a couple of dialysis treatments and fluid he recovered from his symptoms.

In February 2009 he had a prolonged infection with bronchitis. The urea had increased to 40.5 mmol/L and creatinine to 386 mol/L. CRP was 71 mg/L. He was given one dialysis treatment and antibiotics and recovered quickly.

In March 2009, thus one year after withdrawal of dialysis, his renal function was 21 mL/min/1.73 m². His blood pressure (BP) was well controlled with BP 120/60. The s-creatinine was 288 mol/L and electrolytes were good. Cystatin C-estimated GFR was 22 mL/min/1.73 m². In October 2009, thus 18 months after withdrawal, the renal function measured with iohexol clearance was 23 mL/min/1.73 m², the Cystatin C-estimated GFR was 24 mL/min/1.73 m², s-creatinine was 212 mol/L, and the patient was in very good health and working full time. His blood pressure was 123/73 and urine albumin/creatinine ratio 6.3 mg/mmol.

The only disturbing factor was the slightly elevated LD, which was 4.6 cat/L, and elevated ASAT 2.76 cat/L. The CRP was normal, and the hemoglobin values were around 128 g/L, with no signs of hemolysis. A hepatic specialist stated that the enzymes are probably from muscles and most definitely not from the liver.

3. Swedish Renal Registry (SRR) Data

We found 39 patients who had recovered from their renal function, which was defined as dialysis for more than 365 days followed by recovery (SRR, http://www. snronline.se/). The data are presented in Table 2 and reveal that recovery occurred in 14 women and 25 men after 383–2081 days of dialysis treatment. Mean dialysis time was 726 (SD 360) days. A total of 29 patients were treated by means of HD, six with PD, and four with both PD and HD for various lengths of time. The largest groups were those with renovascular disease with hypertension (eight) and chronic renal failure of unknown causes (seven). Of the known diagnoses the most common were hemolytic uremic syndrome (four) and cortical/tubular necrosis (four). Other diagnoses included cholesterol embolism (two), polyarteritis nodosa (two), sclerodermia (two), crescent glomerulonephritis (two), and SLE (two). All patients were alive 3 months after withdrawal, thus it was not done to stop ESRD treatment before impending death.

Time without dialysis treatment after withdrawal ranged from 84 to 6431 days and the mean value was 1415 days, that is, 3. 9 years.

4. Discussion

The Swedish registry revealed that 0.2% of patients recovered from renal function after more than one year of regular dialysis treatment. It may seem a low number. The Swedish Renal Registry (SRR) has been working since 1991. All units performing dialysis and/or kidney transplantation in Sweden report to the registry. Validation of the registry has shown a high accuracy and few patients are missed to be reported. Patients are supposed to be reported as soon as they enter renal replacement therapy by the local nephrologist (registry keyman). The basic criterion for a patient to be reported is that the renal insufficiency is regarded as chronic and based on a chronic kidney disease. When/if a patient has regained renal function, the keyman also reports this to the registry as soon as possible. The registry quality has been maintained by repeated feedback reports to the keymen, by yearly cross-sectional studies of the dialysis population, and by estimation of the number of unknown cases (validation). SRR uses the ERA-EDTA coding system. The patients’ identities are known to us but the medical records have not been scrutinized.

If the rate of recovery from ESRD in the Swedish registry is regarded as low, this could be due to distinct criteria for chronic disease when entering the registry. Data on patients regarded as having an acute renal failure are deleted from the registry.

The data demonstrated that renovascular disease with hypertension was the most common diagnosis and obviously the kidneys can recover with good blood pressure control during dialysis treatment. However, a majority of the patients had no clear diagnosis that explained the reason for the renal failure. The most striking finding was the long renal replacement treatment time, the longest being 5.7 years and the mean treatment time being 2.0 years before renal replacement therapy was withdrawn. Is it difficult to stop dialysis treatment, especially after a long time? Have the kidneys recovered without it being detected? The study by Agraharkar et al. also shows that GFR based on creatinine clearance data at withdrawal was high, 29 mL/min on average with a range from 9 to 51 mL/min [1].

In our case report the diagnosis was thrombotic microangiopathy (TMA) with severe hypertension. The patient was classified as belonging to the group of renovascular diseases with hypertension, which is the largest group. Once his blood pressure had stabilized, the urine production started and the recovery process seemed to progress. A recovery phase of over six months has been described in acute hypertensive diseases by Yaqoob et al. [5].

Our own experience was that it is difficult to detect changes in renal function in dialysis patients. When we started to measure renal function with the injection technique, we found good values, which at first we did not believe to be accurate. However, regular measurements and the use of different methods for assessing renal function made us convinced. Both Cystatin C for estimating renal function and iohexol clearance for measuring function were used together with creatinine clearance. There was also a fear of stopping dialysis due to the risk of high potassium and/or pulmonary edema. We chose to gradually reduce the frequency of dialysis treatment. This seemed safe due to the close monitoring of the patient’s renal function by the nurses and doctors at the dialysis department. The kidney function of our patient is now, 18 months later, in the CKD 4 stage. There is no specific treatment for his original disease and he still needs four different antihypertensive drugs, his blood pressure is depressed, and he has no significant albuminuria. It could be that he already had had a transplant, but the necessary investigations before a patient is accepted for transplantation delayed the procedure, which in this case seemed correct. This observation has been made by others [6].

A third group with recovery was autoimmune diseases and here probably immunosuppressive treatment had importance for the recovery procedure. Spontaneous remissions are found in HUS and membranous glomerulonephritis, which were also identified in the recovery group. The fact that HUS can take a long time before recovery has been described by Brunner et al., who reported two children where recovery occurred after 5 and 7 years and recommended caution before transplantation in this group [7].

Our message is that recovery of renal function could occur even after relatively long time on dialysis. It should particularly be expected in patients with relatively large or increasing urine volumes. Close monitoring and easy access to acute dialysis facilitate the decision to withdraw regular dialysis treatment. For patients who ask whether dialysis treatment is life long, the answer is that a few may recover from renal function and may stop dialysis, even after a relatively long time on dialysis treatment.

Acknowledgments

The authors want to thank the Sophiahemmet Foundation for financial support.

Procedure, purpose, types, side effects, and more

Share on PinterestDialysis can carry out the function of the kidneys if the kidneys no longer work effectively.

A healthy person’s kidneys filter around 120 to 150 quarts of blood each day. If the kidneys are not working correctly, waste builds up in the blood. Eventually, this can lead to coma and death.

The cause might be a chronic, or long-term condition, or an acute problem, such as an injury or a short-term illness that affects the kidneys.

Dialysis prevents the waste products in the blood from reaching hazardous levels. It can also remove toxins or drugs from the blood in an emergency setting.

There are different types of dialysis.

The three main approaches are:

• Intermittent hemodialysis (IHD)
• Peritoneal dialysis (PD)
• Continuous renal replacement therapies (CRRT)

The choice will depend on factors such as the patient’s situation, availability, and cost.

Intermittent hemodialysis

In hemodialysis, the blood circulates outside the body. It goes through a machine with special filters.

The blood comes out of the patient through a flexible tube known as a catheter. The tube is inserted into the vein.

Like the kidneys, the filters remove the waste products from the blood. The filtered blood then returns to the patient through another catheter. The system works like an artificial kidney.

Those who are going to have hemodialysis need surgery to enlarge a blood vessel, usually in the arm. Enlarging the vein makes it possible to insert the catheters.

Hemodialysis is usually done three times a week, for 3 to 4 hours a day, depending on how well the kidneys work, and how much fluid weight they have gained between treatments.

Hemodialysis can be done in a special dialysis center in a hospital or at home.

People who have dialysis at home, or their caregiver, must know exactly what to do.

If a person does not feel confident doing dialysis at home, they should attend sessions at the hospital.

Home hemodialysis is suitable for people who:

• have been in a stable condition while on dialysis
• do not have other diseases that would make home hemodialysis unsafe
• have suitable blood vessels for inserting the catheters
• have a caregiver who is willing to help with hemodialysis

The home environment must also be suitable for taking hemodialysis equipment.

Peritoneal dialysis

While hemodialysis removes impurities by filtering the blood, peritoneal dialysis works through diffusion.

In peritoneal dialysis, a sterile dialysate solution, rich in minerals and glucose, is run through a tube into the peritoneal cavity, the abdominal body cavity that surrounds the intestine. It has a semi-permeable membrane, the peritoneal membrane.

Peritoneal dialysis uses the natural filtering ability of the peritoneum, the internal lining of the abdomen, to filter waste products from the blood.

The dialysate is left in the peritoneal cavity for some time, so that it can absorb waste products. Then it is drained out through a tube and discarded.

This exchange, or cycle, is normally repeated several times during the day, and it can be done overnight with an automated system.

The elimination of unwanted water, or ultrafiltration, occurs through osmosis. The dialysis solution has a high concentration of glucose, and this causes osmotic pressure. The pressure causes the fluid to move from the blood into the dialysate. As a result, more fluid is drained than is introduced.

Peritoneal dialysis is less efficient than hemodialysis. It takes longer periods, and it removes around the same amount of total waste product, salt, and water as hemodialysis.

However, peritoneal dialysis gives patients more freedom and independence, because it can be done at home instead of going to the clinic several times each week. It can also be done while traveling with a minimum of specialized equipment.

Before starting peritoneal dialysis, the patient needs a small surgical procedure to insert a catheter into the abdomen. This is kept closed off, except when being used for dialysis.

There are two main types of peritoneal dialysis:

Continuous ambulatory peritoneal dialysis (CAPD) requires no machinery, and the patient or a caregiver can do it.

The dialysate is left in the abdomen for up to 8 hours and then replaced with a fresh solution straight away. This happens every day, four or five times per day.

Continuous cyclic peritoneal dialysis (CCPD), or automated peritoneal dialysis uses a machine to exchange the fluids. It is generally done every night, while the patient sleeps.

Each session lasts from 10 to 12 hours. After spending the night attached to the machine, most people keep the fluid inside their abdomen during the day. Some patients may need another exchange during the day.

Peritoneal dialysis is a suitable option for patients who find hemodialysis too exhausting, such as elderly people, infants, and children. It can be done while traveling, so it is more convenient for those who work or attend school.

Continuous renal replacement therapy

Dialysis can be intermittent or continuous.

While a session of intermittent dialysis lasts for up to 6 hours, continuous renal replacement therapies (CRRT) are designed for 24-hour use in an intensive care unit (ICU).

There are different types of CRRT. It can involve either filtration or diffusion. It is better tolerated than intermittent dialysis, because the solute or fluid removal is slower. This leads to fewer complications, for example, a lower chance of hypotension.

Temporary dialysis

Sometimes dialysis is given for a limited period of time.

People who may benefit from temporary dialysis include those who:

Risks and complications include:

In some cases, the kidneys recover and do not need further treatment.

What is it, Causes, Dialysis & More

Overview

What is end-stage renal disease?

End-stage kidney disease (ESKD), or kidney failure, is the fifth and final stage of chronic kidney disease (CKD) progression. With chronic kidney disease, your kidneys can’t do their day-to-day job. When they fail, you need treatment either dialysis or a kidney transplant to survive.

What do the kidneys do?

The kidneys are bean-shaped organs, located deep inside the body toward the back, down near the hips. Most people have two kidneys. But some people are born with only one kidney, or only one that works. Other people have a single kidney because they donated one or had one removed for another health reason. In most cases, one kidney can still do everything your body needs.

The kidneys:

• Filter blood (about a half-cup per minute) to remove waste, extra water and acid.
• Help the body maintain a healthy balance of water, salt and minerals such as potassium, calcium and magnesium.
• Make urine, or pee, so the body can remove waste.
• Make hormones to help control blood pressure, keep bones strong and create red blood cells to prevent anemia.

Symptoms and Causes

What causes kidney failure?

Kidney disease is caused by many different health problems that can damage the kidneys. The damage can take place all at once or a little bit at a time over many years. Eventually, kidney disease can lead to kidney failure.

Common causes of kidney disease include:

What are the symptoms of end-stage renal disease?

Early kidney disease often has no symptoms. Some people may not even know they have kidney disease until their kidneys fail.

If your kidneys begin to fail, you may experience:

• Confusion.
• Itchiness all over.
• Lack of appetite.
• Metallic taste in your mouth.
• Muscle cramps or muscle jerking.
• Nausea and vomiting.
• Shortness of breath.
• Swelling in your feet or ankles.
• Too much or too little urine production.
• Trouble sleeping, or sleeping too much.

If you develop any of these symptoms, you should contact a healthcare provider immediately.

What are the complications of renal failure?

End-stage renal failure can cause complications and emergencies that require treatment, including:

• Anemia (not enough red blood cells to carry oxygen throughout the body. )
• Bone disease.
• Brain damage.
• Edema (swelling)
• Fluid in and around the lungs.
• High levels of certain minerals (potassium or phosphorus).
• Infections.
• Nerve damage.
• Seizures.
• Stroke.

Diagnosis and Tests

What tests should I have for kidney disease?

People with chronic kidney disease usually see a kidney specialist called a nephrologist. This healthcare provider takes blood tests at a set schedule to measure levels of:

• Albumin (protein).
• Calcium (mineral), phosphorus, parathyroid hormone (bone markers++)++
• Cholesterol (fat).
• Creatinine (muscle waste product).
• Magnesium (mineral).
• Potassium and sodium (electrolytes).
• Red blood cells and complete blood count (CBC).

Management and Treatment

Can doctors cure kidney failure?

Healthcare providers can treat, slow or stop kidney disease but can’t cure kidney failure. A person with end-stage kidney disease needs dialysis or a kidney transplant to survive.

When do you know you need dialysis or a kidney transplant?

Your healthcare provider will calculate a special score called the estimated glomerular filtration rate, or eGFR. This score helps the provider track the severity of kidney disease over time. It starts at 100 (highest kidney function) and goes down to 0 (no kidney function). A score below 15 marks kidney failure and the need for dialysis or kidney transplant.

Healthcare providers determine the filtration rate based on your:

• Age.
• Creatinine blood levels.
• Body size.
• Gender.

What is dialysis?

Dialysis takes over the work of the kidneys to keep your body in balance. It has no effect on kidney function. There are two common types:

• Hemodialysis: A machine called a hemodialyzer removes blood from your body, filters it and returns the cleaned blood to your body. Healthcare providers need to use blood vessels in your arm to transfer the blood.
• Peritoneal dialysis: This treatment cleans the blood while it’s still in your body. To start, healthcare providers place a plastic tube in your belly. They then pump in a solution that collects extra fluid and waste. They remove the solution at the end of the cleaning.

Where do I get dialysis?

You can receive dialysis in a hospital, in a dialysis clinic or at home. Your healthcare provider will help you decide which option is best for you.

How long does dialysis take?

Usually, each hemodialysis treatment lasts about four hours. Most people receiving hemodialysis need it three times a week. A peritoneal dialysis treatment takes 30 to 40 minutes and should get done several times a day.

Your nephrologist will determine what type of dialysis you need based on:

• Amount of waste in your body.
• How much fluid you have.
• Your kidney function.
• Your size.

A person waiting for a kidney transplant needs dialysis treatments right up to the time of surgery.

What is a kidney transplant?

A kidney transplant is an operation where surgeons replace the diseased kidney with a new one placed in the groin area. The kidney can come from someone who has died or from a living donor. Remember, most people have two kidneys and can live just fine with one healthy kidney.

Your healthcare team will perform tests to determine if the donor kidney is a good match. To prevent your body from rejecting a new kidney, you will need to take special drugs. These drugs are called anti-rejection medications or immunosuppressants.

After a successful transplant, the donated kidney will start filtering blood and removing waste.

Prevention

Can I prevent kidney failure?

The best way to prevent end-stage renal disease is to manage the disease harming your kidneys, especially high blood pressure or diabetes. Doing so will limit the amount of damage done to your kidneys.

Outlook / Prognosis

What is the outlook for a person with kidney failure?

Healthcare providers can’t cure kidney failure, and the disease is life-threatening. But dialysis or a kidney transplant can help you live longer and manage any symptoms or complications. You can also do the things you enjoy.

Living With

Should I change my lifestyle to manage kidney failure?

People with severe kidney disease (even those on dialysis) should:

• Exercise.
• Limit fluids.
• Limit foods that contain phosphorus, potassium or sodium (salt).

A dietician can help you plan proper nutrition for kidney disease.

Can I still work if my kidneys are failing?

Many people with kidney failure keep working. It may make you feel more normal and productive. And it can provide insurance to cover your health costs.

Your healthcare providers can help you plan a treatment schedule that fits your work needs. You can even ask your healthcare provider for a social worker to help you talk with your employer. For example, if you’re on peritoneal dialysis and do it yourself, you’ll need access to a clean place at work. If you’re on hemodialysis, your employer should know that you can’t lift heavy things.

If you can’t work, government and private programs can help. They can provide money, health insurance and transportation to doctors’ appointments and treatments. A social worker can help you find such programs and apply.

A note from Cleveland Clinic

End-stage renal disease is the last stage of chronic kidney disease. It marks the point when kidney function drops to very low levels. Kidney failure failure is life threatening, but dialysis or transplantation can relieve weakened kidneys. If you have kidney disease, a healthcare provider can help you manage the cause and watch your kidney function.

CRRT dialysis in the ICU — what patients and families want to know – The Reporter

Ashita Tolwani, M.D., with a CRRT machine in UAB’s Medical Intensive Care Unit. The bag at center under the machine is filled with Prismocitrate 18, the anticoagulant that Tolwani developed that is now used in continuous dialysis around the world.Florida orange growers may name an annual Citrus Queen, but UAB has the all-time Citrate Queen. That’s one of the titles — the other is CRRT Queen — bestowed by colleagues on Ashita Tolwani, M.D., an international expert on continuous renal replacement therapy (CRRT) and the holder of the DCI Edwin A. Rutsky, M.D., Distinguished Endowed Professorship in Nephrology in the UAB Division of Nephrology.

Unlike regular dialysis, which takes 3-4 hours, continuous dialysis runs 24 hours a day and is increasingly used in intensive care units for patients with acute kidney failure because it is far gentler on the body. A 2012 article by Tolwani in the New England Journal of Medicine demonstrated that CRRT provides more gentle solute (waste) and fluid removal than standard dialysis techniques. This is crucial, because the mortality rate for critically ill patients with acute kidney failure who need dialysis has been reported to be higher than 50 percent. But CRRT is also a complicated therapy that requires special expertise on the part of physicians and nurses to use properly.

Citrate is the yellowish substance you’ve seen at the bottom of the tubes your doctor’s office uses to collect blood, in order to keep that blood from coagulating, or clotting. In 2004, Tolwani developed a new kind of anticoagulant solution based on citrate that has helped make CRRT safer and simpler, allowing it to spread worldwide. That anticoagulant, Prismocitrate 18, is now used in Europe, Canada, India, Australia, New Zealand and most of the rest of the planet. Approval from the U.S. FDA is still pending, although UAB and other U.S. hospitals formulate the compound in their pharmacies. (Meanwhile, Tolwani used royalties from sales of the anticoagulant to start an innovation fund that backs new kidney-related therapies.)

UAB has one of the busiest CRRT programs in the world. “We provide more than 6,000 patient-days of treatment each year,” Tolwani said. She had so many requests from other physicians wanting to learn her techniques that she started an annual training symposium at UAB that attracts doctors throughout the United States, Mexico, India and other countries and runs a constant waiting list.

CRRT is becoming more familiar to doctors and patients alike. “I’m constantly getting email from both critical care and kidney doctors around the world,” Tolwani said. So we asked her to explain the therapy, when it is used and the most common questions she hears from patients and families.

How do you explain continuous renal replacement therapy (CRRT) to your patients?

Continuous renal replacement therapy is a special type of dialysis that we do for unstable patients in the ICU whose bodies cannot tolerate regular dialysis. It is a very different type of dialysis from the routine type that patients may be familiar with, and it requires special skills and expertise. Regular hemodialysis is meant to be mostly an outpatient procedure. It is done usually three times a week for three to four hours at a time. The flow rates used to clear waste products and remove fluid from the patient are very fast, potentially putting stress on a patient’s heart and blood pressure. If a patient already has a low or unstable blood pressure or has heart issues, he or she will not tolerate regular dialysis. CRRT is a slower type of dialysis that puts less stress on the heart. Instead of doing it over four hours, CRRT is done 24 hours a day to slowly and continuously clean out waste products and fluid from the patient. It requires special anticoagulation to keep the dialysis circuit from clotting.

Who needs to be on dialysis 24 hours a day?

Today we can keep patients alive longer with multiple medical procedures and medications which unfortunately can increase the risk of acute kidney injury (AKI). One such example is a procedure known as ECMO [a type of heart-lung bypass machine].

About 20% of patients in the hospital setting have AKI; in the ICU it’s about 65%. When patients are on ventilators or require antibiotics because they have severe infections — sepsis — or need medications to raise their blood pressure, called vasopressors, those can all cause AKI.

Up to 25% of ICU patients with AKI may require dialysis to remove waste products and fluid that build up when the kidneys are not working. The preferred choice of dialysis for these critically ill patients is CRRT. It allows doctors to give patients the fluids, nutrition, antibiotics and other medications they need without worrying about the accumulation of waste products and fluid from the failing kidneys.

How long do patients stay on continuous dialysis?

This is the most common question I get asked by patients and families. Their biggest concern is the dialysis machine and the recovery of kidney function. Maybe that’s because they have heard of dialysis and can relate to it better than the other therapies patients receive in the ICU setting.

CRRT is used until patients start showing signs of their own kidneys recovering — or until they have more stable blood pressure and can tolerate regular dialysis.

What are the signs the kidneys are recovering?

The first sign is when a patient starts making urine. Most of the patients on CRRT are unable to make urine because of their kidney failure. However, even if the patient starts making urine, the filtrating capacity of the kidney takes a longer time to recover. It can be weeks or months before the kidney is able to filter solutes and get rid of wastes.

Families often ask, “How’s the creatinine doing?” Creatinine is a toxin and waste product that the kidneys remove and so a creatinine higher than the normal range indicates the kidneys are damaged and cannot filter solutes and toxins.  When a patient is treated with CRRT, the machine removes waste products and toxins and so the creatinine levels become lower and in the normal range. But this does not reflect what the patient’s kidneys are doing.  Therefore, I first teach families to focus on how much urine the patient is making. Once a patient is making more than 500 ml to 1,000 ml of urine a day, we can test the urine to see if it is actually filtering out the toxins, indicating that the kidneys are trying to recover.  Once the kidneys are able to filter the waste products so they do not build up to dangerous levels in the body, dialysis can be discontinued.

Families will also say, “They’re not drinking anything. That’s why they’re not making urine.” I explain that once the tubules in the kidney are damaged and not working, giving more fluids isn’t going to help and can make things worse. Even if dehydration was a cause of the original injury, it’s not dehydration anymore once the tubules are damaged. Furthermore, patients are still getting fluids from intravenous medications and nutrition. If the kidneys have shut down, the excess fluid has nowhere to go and accumulates in the body leading to fluid in the lungs, swelling of the body and even heart issues.

It may take three months or longer to recover from acute renal failure. If you have healthy kidneys before entering the hospital, you have a greater than 90% chance of recovering. If you already have chronic kidney damage, you are less likely to recover.

So how can I keep my kidneys healthy?

I always tell my patients to stay hydrated. Many medications that are normally safe become dangerous to your kidneys when you are dehydrated and the blood supply to the kidneys decreases. Examples are ACE inhibitors and ARBs, two common heart medications used for blood pressure control and both heart and kidney issues.

If you are dehydrated, even something as simple as ibuprofen can shut down your kidneys. Many medical conditions such as high blood pressure and poorly controlled diabetes can permanently damage the kidneys as well.  As a result, it is very important to keep high blood pressure and diabetes controlled.

What else do your patients or families want to know?

Family members always ask, “Can I just give my kidney right now for a transplant?” Unfortunately, in the state the patient is in to be in the ICU, they would not survive a transplant operation. I tell them, “If they don’t get their kidney function back in three months, then we’ll consider kidney transplantation. Right now, they need to recover.”

You also do research on CRRT — what are the questions that need to be answered?

Because we have so much experience with CRRT at UAB, we help set what the research agenda should be. Right now, that is looking at the most appropriate dose of CRRT and early versus late initiation of the therapy.

Control over fluid intake

Fluid intake should be carefully monitored in dialysis patients. This is especially important if your kidneys are not making any urine at all. Patients on hemodialysis generally need to monitor their fluid intake more closely than patients on peritoneal dialysis.

Control your thirst

The best way to reduce your fluid intake is to reduce the feeling of thirst caused by your intake of sodium in your food.Excessive sodium in your diet is the reason you drink too much fluids.

Sodium is found in salt. Most canned foods and frozen meals are high in sodium. Avoid salty foods like potato chips in favor of low sodium foods.

The largest amount of salt consumed is the addition of salt to food during preparation or consumption. Dialysis patients should aim to consume half as much salt as other people.

Monitor fluid consumption

You can reduce your fluid intake by using small cups or glasses. Any food that is liquid at room temperature contains water. For example: soups, milk, yoghurts, jellies and ice cream. Many fruits and vegetables also contain high amounts of water. These include melons, watermelons, grapes, apples, oranges, tomatoes, lettuce, and celery. All of these foods increase fluid intake.

Management of fluid intake during hemodialysis

Fluid can build up between hemodialysis sessions, causing swelling and weight gain.Excessive fluid volume affects blood pressure and can make it difficult for the heart to function. You should aim for a weight gain of about 0.5 kg per day between dialysis sessions.

Dry weight is the weight of your body after a hemodialysis session when all excess fluid has been removed from your body. If you allow too much fluid to build up between sessions, it will be more difficult to achieve dry weight. This increases the risk of dialysis intolerance (hypotension, cramping, etc.). Your dry weight can change over time if your body weight changes.

Management of fluid intake in peritoneal dialysis

Fluid intake is not as limited as in hemodialysis patients, but you should still monitor it to avoid fluid retention problems.

Ultrasound examinations

Sodium level in dialysate for chronic hemodialysis

What is the problem?

The kidneys control the balance of salt and water in the body by regulating the production of urine. When the kidneys stop working, urination stops or becomes insufficient, and the water-salt balance is maintained with dialysis.Physicians managing hemodialysis patients should select an appropriate amount of sodium for use in dialysis fluids used to cleanse the patient’s blood. If the sodium level in these fluids is too high, it can cause the patient to feel thirsty after treatment, excessive water intake and fluid overload by the time the next treatment is started, which can lead to heart damage. On the other hand, if the sodium level in dialysis fluids is too low, the patient may experience seizures and a drop in blood pressure, which causes discomfort and can also damage the heart.The “correct” dialysis fluid sodium level is unknown.

What have we done?

We pooled all studies of people treated with hemodialysis that compared results between people who received low sodium in dialysis fluid and people who received higher sodium.

What have we found?

We found 12 studies comparing low dialysis fluid sodium levels with neutral or high sodium levels.Many studies were conducted before 2000, research technologies and patients are not always relevant today. Most of them were short-term, lasting only a few weeks. Our main findings in these studies were that low sodium levels in dialysis fluid improved blood pressure and decreased salt and water inflow between dialysis sessions, which is probably good, but increases the number of cramps and episodes of low blood pressure experienced by patients. during dialysis, which is definitely bad.The studies did not provide us with enough information about the participating patients to know which patients might benefit from low sodium dialysis and which patients might benefit.