Renal Disease

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Questions Received:

  1. Can the sweat glands be used to replace dialysis in patients with renal failure?

  2. Is this still considered the standard of care: renal insufficiency defined as serum creatinine greater that 2.5 u/dL? Or is a level of 3.0 now considered acceptable?

  3. My mother has a creatinine clearance of 13.09 ml/min and serum creatinine of 4.59 mg/dl. Can you tell me what she can or should do to delay the onset of ESRD (I believe dialysis is required if Creatinine Clearance goes <10 ml/min). I am looking for advice on medication that should be recommended, etc. She lives in Pakistan where the cost of healthcare can be prohibitive or limited. I would like your advise which I will follow up with a local physician.

  4. What treatment is available for Calciphalaxus?

Responses:

Can the sweat glands be used to replace dialysis in patients with renal failure?

10th May 1998

This question has particular significance in countries where the cost of dialysis or kidney transplantation is beyond the means of the majority of the people. The skin is sometimes referred to as the 'third kidney' because of its ability to excrete some of the body's waste products, and sweat glands have some parallels with the nephrons of the kidneys in the way that they respond to controlling influences such as antidiuretic hormone. We tend to think of sweat glands in the role of temperature regulation, but perhaps they could be stimulated to take on more of an excretory role in patients with renal disease?

The sweat glands of patients in renal failure tend to be smaller and less active than those in healthy subjects (Shankle, Azen, and Landing, 1982), with the result that the skin tends to become dry. The sweat glands are also less responsive to 0.05% pilocarpine (Park et al, 1995), but become more sensitive to adrenaline (Teodosieva and Teodosiev, 1980). In patients with renal failure, the sweat weight was significantly lower than in healthy controls, regardless of whether they were undergoing dialysis or not. Sweat potassium concentration was significantly higher in patients with renal failure than in healthy controls, while the concentrations of sodium and chloride ions were similar (Yosipovitch et al, 1994).

Can sweat glands be trained or stimulated to develop more sweat in order to assist kidney patients with nitrogenous excretion? It appears that sweat glands are indeed trainable. When healthy subjects and patients with renal insufficiency were exposed to saunas and hot tubs sweat output was significantly increased (Koban et al, 1987), and the sweat of patients with renal insufficiency contained more solutes (nitrogen metabolites, electrolytes, and acid) than that of normal people. However, the quantity of medium sized molecules (1,100 to 2,050 Dalton) in sweat of patients with renal failure is similar to that in the ultrafiltrate of patients undergoing haemodyalysisis, and does not exceed normal values (Koban et al, 1989). Sweat glands can be trained to become more active by immersion of an arm in hot water at 43 degrees C. However, under these conditions it was found that sweat electrolytes decreased (Ogawa, Asayama, and Miyagawa, 1982). Sweat production can also be enhanced by physical training (Taylor, 1986).

So it does appear that sweat glands can be encouraged to take on a greater excretory role in patients with renal disease. Several stimulatory strategies are possible - drug treatment, exposure to saunas and hot tubs, and exercise - but the benefits would have to be weighed against the additional stresses being placed on the patients. At this time, it appears that sweat gland activity can provide only a partial replacement for dialysis, but nonetheless an avenue worth exploring further.

References

Is this still considered the standard of care: renal insufficiency defined as serum creatinine greater that 2.5 u/dL? Or is a level of 3.0 now considered acceptable?

13th April 1999

The normal range for serum creatinine is 0.6 to 1.5 mg per 100ml (60 - 130 m mol/L). Renal insufficiency can have a gradual onset and symptoms may not occur until a substantial proportion of kidney function has been lost. However, serum creatinine levels begin to rise at an earlier stage, and this measure is considered to be a reliable indicator of renal function (see graph). It is somewhat arbitrary to set a threshold between normality and renal insufficiency, because individual circumstances would have to be taken into account and the risein creatinine levels is very gradual at first, but a figure of 2.5 mg per 100 ml (221 m mol/L) could be taken as an indication of an early stage in renal insufficiency.

Creatinine is generated by muscle cells as a by-product of creatine metabolism. The amount produced is proportional to the muscle mass. It is transported via the blood to the kidneys, where it is excreted in the urine. Studies of creatinine levels can give an insight into renal function, particularly the glomerular filtration rate, because blood levels of creatinine remain fairly constant. In this it differs from urea, the level of which varies quite widely depending on protein intake with the diet and the level of metabolism. Estimation of creatinine clearance requires the collection of all urine produced over 24 hours. A specimen of venous blood is also required to estimate plasma creatinine levels. A 24-hour specimen of urine is collected so that the total daily amount of creatinine excreted may be measured and the excretion rate per minute calculated. In some types of renal disease, the creatinine clearance rate falls, and the plasma level rises correspondingly.

Our thanks to Stephen Bottomley, Senior Biochemist, Royal Devon & Exeter Healthcare N.H.S. Trust, Wonford, Exeter EX2 5DW for help with this answer.

My mother has a creatinine clearance of 13.09 ml/min and serum creatinine of 4.59 mg/dl. Can you tell me what she can or should do to delay the onset of ESRD (I believe dialysis is required if Creatinine Clearance goes <10 ml/min). I am looking for advice on medication that should be recommended, etc. She lives in Pakistan where the cost of healthcare can be prohibitive or limited. I would like your advise which I will follow up with a local physician.

31st May 1999

Useful advice for kidney patients who have little or no access to renal healthcare facilities is provided by the World Kidney Fund at www.worldkidneyfund.org

There are several measures which can help to delay the need for dialysis:

Reduction of Blood Pressure

The progression of renal failure can be slowed by lowering blood pressure. Blood pressure should be maintained below 130/85 mm Hg if possible (McCarthy, 1999). Angiotensin-converting enzyme inhibitors have been shown to be more beneficial than other antihypertensives in this situation (Lafayette, 1995; Hood and Gennari, 1996; Bretzel, 1997; el Nahas and Coles, 1997; Giatras, Lau, and Levey, 1997; Ruggenenti and Remuzzi, 1997; Aradhye, 1998; Rahman and Smith, 1998; Barrett, 1999). However, renal function should be checked after two weeks treatment with an angiotensin-converting enzyme inhibitor and if there is deterioration the treatment should be stopped (el Nahas and Coles, 1997).

Low Protein Diet

Low-protein diets (10-20 g per day) can slow down the deterioration of renal function (ter Wee and Donker, 1992; Lafayette, 1995; Aradhye, 1998; Rahman and Smith, 1998). However, the nutritional status of the patient must be reviewed regularly if this approach is taken (el Nahas and Coles, 1997). Supplementation of essential amino acids may be required.

Glycaemic Control in Patients with Diabetes

Careful glycaemic control in patients with diabetes can slow down the progression of chronic renal disease (Lafayette, 1995; Hood and Gennari, 1996; Rahman and Smith, 1998).

Additional Measures

A variety of clinical problems such as electrolyte imbalances, secondary hyperparathyroidism, and anaemia may develop in patients with progressive renal failure, and these have to be treated as they occur (Aradhye, 1998; Rahman and Smith, 1998; McCarthy, 1999). Maintaining the haemoglobin level at 10 to 12 g/dL with iron supplementation, erythropoietin, or androgens can improve quality of life and help to prevent cardiac disease (Barrett, 1999; McCarthy, 1999). Treatment of raised lipid levels in the blood might reduce the effects of cardiovascular disease on renal function (ter Wee and Donker, 1992; Barrett, 1999). Care should be taken to avoid any drugs or radiographic materials that might be damaging to the kidneys (Aradhye, 1998). Urinary tract infections should be treated promptly.

References

We wish to thank Dr Peter Bisson for help in preparing this answer.

What treatment is available for Calciphalaxus?

15th August 2000

(Calciphylaxis is also referred to as Uremic Gangrene Syndrome)

Calciphylaxis is a rare condition in which small blood vessels in the skin become calcified. As a consequence, purple-coloured skin lesions appear which progress to painful nonhealing ulcers and sepsis (Budisavljevic, Cheek, and Ploth, 1996; Ledbetter, Khoshnevis, and Hsu, 2000). Gangrene of fingers and toes frequently requires amputation, and the condition can be fatal. Calciphylaxis is most commonly associated with advanced kidney disease, particularly in patients with disturbed calcium and phosphorus metabolism and elevated levels of parathyroid hormone. The increasing use of calcium salts as a phosphate binder in dialysis patients might be linked with the increased incidence of calciphylaxis in recent years (Zacharias, Fontaine, and Fine, 1999).

Treatment is usually by giving phosphate-binding antacids, by partial or complete removal of the parathyroid glands, and by the avoidance of challengers such as Vitamin D or local tissue trauma (Roe et al, 1994; Kriskovich, Holman, and Haller, 2000; Ledbetter, Khoshnevis, and Hsu, 2000). Opinions differ about the value of treating with corticosteroids (Elamin and McDonald, 1996; Worth, 1998). It is reported that hyperbaric oxygen therapy (treatment in a pressure chamber at raised oxygen levels) has helped to heal persistent calciphylactic skin ulcers (Dean and Werman, 1998). The severe pain associated with calciphylaxis has been treated in some cases by neurolytic lumbar sympathetic blockade (Green, Green, and Minott, 2000).

References

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