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Chronic renal failure

Chronic renal failure (CRF, or "chronic kidney failure", CKF) is a slowly progressive loss of renal function over a period of months or years and defined as an abnormally low glomerular filtration rate, which is usually determined indirectly by the creatinine level in blood serum. more...

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CRF that leads to severe illness and requires some form of renal replacement therapy (such as dialysis) is called end-stage renal disease (ESRD).

Signs and symptoms

Initially it is without symptoms and can only be detected as an increase in serum creatinine. As the kidney function decreases:

  • Blood pressure is increased (hypertension)
  • Urea accumulates, leading to uremia (symptoms ranging from lethargy to pericarditis and encephalopathy)
  • Potassium accumulates in the blood (known as hyperkalemia with symptoms ranging from malaise to fatal cardiac arrhythmias)
  • Erythropoietin synthesis is decreased (leading to anemia causing fatigue)
  • fluid volume overload - symptoms may range from mild edema to life-threatening pulmonary edema
  • Hyperphosphatemia - due to reduced phosphate excretion, associated with hypocalcemia (due to vitamin D3 deficiency) and hyperparathyroidism - leads to renal osteodystrophy and vascular calcification

CRF patients suffer from accelerated atherosclerosis and have higher incidence of cardiovascular disease, with a poorer prognosis.

Diagnosis

In many CRF patients, previous renal disease or other underlying diseases are already known. A small number presents with CRF of unknown cause. In these patients, a cause is occasionally identified retrospectively.

It is important to differentiate CRF from acute renal failure (ARF) because ARF can be reversible. Abdominal ultrasound is commonly performed, in which the size of the kidneys are measured. Kidneys in CRF are usually smaller (< 9 cm) than normal kidneys with notable exceptions such as in diabetic nephropathy and polycystic kidney disease. Another diagnostic clue that helps differentiate CRF and ARF is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). If these levels are unavailable (because the patient has been well and has had no blood tests) it is occasionally necessary to treat a patient briefly as having ARF until it has been established that the renal impairment is irreversible.

Numerous uremic toxins (see link) are accumulating in chronic renal failure patients treated with standard dialysis. These toxins show various cytotoxic activities in the serum, have different molecular weights and some of them are bound to other proteins, primarily to albumin. Such toxic protein bound substances are receiving the attention of scientists who are interested in improving the standard chronic dialysis procedures used today.

Causes

The most common causes of CRF in North America and Europe are diabetic nephropathy, hypertension, and glomerulonephritis. Together, these cause approximately 75% of all adult cases. Certain geographic areas have a high incidence of HIV nephropathy.

Read more at Wikipedia.org


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Coenzyme Q10 for chronic renal failure
From Townsend Letter for Doctors and Patients, 10/1/05 by Alan R. Gaby

Ninety-seven patients (mean age, 48 years) with chronic renal failure (serum creatinine > 5 mg/dl), with a history of declining renal function for at least 12 weeks, were randomly assigned to receive, in double-blind fashion, water-soluble coenzyme Q10 (CoQ10; 60 mg, 3 times per day orally) or placebo for 12 weeks. The 45 patients who were receiving hemodialysis at the start of the study were encouraged to decrease the frequency or stop dialysis if there was an increase in urine output and a decrease in serum creatinine of more than 2 mg/dl. In the patients receiving hemodialysis and CoQ10, the mean serum creatinine concentration decreased from 9.5 to 6.7 mg/dl; mean BUN decreased from 88.2 to 79.8 mg/dl; mean creatinine clearance increased from 40 to 54.9 ml/min; and 24-hour urine output increased from 1,300 to 1,920 ml. Renal function tended to worsen in hemodialysis patients receiving placebo, and the differences in the changes between groups were significant (p < 0.01 to p < 0.001). Significant improvements in each of these parameters relative to the placebo group were also seen in the non-dialysis patients treated with CoQ10. The number of patients receiving dialysis decreased from 21 to 12 in the CoQ10 group, and remained unchanged at 24 in the placebo group (p < 0.02). Eighty-one percent of the patients receiving CoQ10 had a positive response to treatment.

Comment: These results suggest that CoQ10 can improve renal function and reduce the need for dialysis in patients with chronic renal failure. The public-health implications of this study are enormous, considering that chronic renal failure is a serious and debilitating disease and that the annual cost of dialysis in the United States is more than $22 billion.

According Dr. Singh, the lead author of this study (Interview with Kirk Hamilton; Clinical Pearls News, August, 2001, pp. 128-9), CoQ10 is usually effective if pre-treatment urine output, with or without furosemide, is at least 1,000 ml/day. However, if urine output is less than 500 ml/day, then CoQ10 usually does not work, presumably because the kidney has been irreversibly damaged. Dr. Singh recommends that that all patients with renal failure take 180 mg/day of water-soluble CoQ10 if their urine output is greater than 500 ml/day on dialysis. If urine output increases to 1,000 ml/day within 12 weeks, then CoQ10 is likely to be effective. Patients should be able to stop dialysis within 12-48 weeks if the urine output goes above 1,500 ml/day. If urine output does not increase in 12 weeks, then CoQ10 is unlikely to be effective.

While the mechanism by which CoQ10 improves renal function is not clear, it may work by improving cellular bioenergetics. Large controlled trials are urgently needed.

Singh RB, et al. Randomized, double-blind, placebo-controlled trial of coenzyme CoQ10 in patients with end-stage renal failure. J Nutr Environ Med 2003; 13:13-22.

COPYRIGHT 2005 The Townsend Letter Group
COPYRIGHT 2005 Gale Group

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