Almost 20 million adult Americans have chronic kidney disease and most don't know it; another 20 million are at high risk for it

End-stage kidney failure is increasing by 2% a year in the U.S. where
    300,000 Americans are on dialysis
    80,000 Americans are living with transplanted kidneys

The good news, according to the National Kidney Foundation, is that early diagnosis and treatment can slow progression of a disease that usually displays no serious symptoms until the kidneys have suffered severe damage.* Unfortunately, at that late point, one has to resort to kidney dialysis or transplant to filter the blood-remove the waste products of the body's work (metabolism) and poisons we cannot live with.

The key: persons who are at risk, such as those of us with diabetes, high blood pressure, the elderly, or those with strong family histories of kidney disease need easy urine and blood tests to tell if they have impaired kidney function.

How does testing work?

- People with kidney disease lose an excess of protein in their urine. This can be detected by a simple urine dipstick test. However, the albumin-specific kind of test or sending the urine to a laboratory for the same is preferred because microscopic amount of albumin in the urine--microalbuminuria--is the important early warning sign. In other words, regular dipstick tests like the kind often used for pregnant women may not appear positive until later.

- A glomerular filtration rate (GFR) test may be needed to estimate how well the kidneys are filtering. A blood test that measures levels of a body metabolite (a product of metabolism), creatinine is part of this test.

- The American Diabetes Association recommends yearly urine tests for microalbuminuria in most diabetics.

Four therapies are available to slow kidney damage

- Angiotensin II receptor blockers (a medication) can slow kidney failure by about two (2) years in people with advanced disease; proponents suggest these drugs work even better if taken in the earlier stages of chronic renal disease. They work by relaxing essential blood vessels in the kidneys, and are similar to a type of blood pressure medicine called ACE-inhibitors.
- Strict blood pressure control is vital.
- In diabetics, strict blood sugar control protects the kidneys.
- Low-protein diets are often recommended, although studies of whether they help have had mixed results.

To track how well therapy is working, patients need these blood and urine tests repeated periodically-at least yearly, and more often if the renal function deteriorates rapidly, or if the GFR drops below 60 mL/min/m2, which separates mild disease from more serious organ damage.

For people whose first tests show they don't yet have kidney disease, the Kidney Foundation still is studying how often screening test should be offered.
From the new guidelines for the early detection of kidney disease, published in the American Journal of Kidney Diseases (February, 2002).

* Medical Literature from THE MERCK MANUAL, Sec. 17, Ch. 222, Renal Failure

For substances that are excreted mainly through distal nephron secretion (eg, K), adaptation usually produces a normal plasma concentration until advanced failure occurs.

Despite a diminishing GFR, Na and water balance is well maintained by increased fractional excretion of Na and a normal response to thirst. Thus, the plasma Na concentration is typically normal and hypervolemia is infrequent despite unmodified dietary intake of Na. However, imbalances may occur if Na and water intakes are very restricted or excessive.

Symptoms and Signs

Patients with mildly diminished renal reserve are asymptomatic, and renal dysfunction can be detected only by laboratory testing. A patient with mild to moderate renal insufficiency may have only vague symptoms despite elevated BUN and creatinine; nocturia is noted, principally due to a failure to concentrate the urine during the night. Lassitude, fatigue, and decreased mental acuity often are the first manifestations of uremia.

Neuromuscular features include coarse muscular twitches, peripheral neuropathies with sensory and motor phenomena, muscle cramps, and convulsions (usually the result of hypertensive or metabolic encephalopathy). Anorexia, nausea, vomiting, stomatitis, and an unpleasant taste in the mouth are almost uniformly present. Malnutrition leading to generalized tissue wasting is a prominent feature of chronic uremia. In advanced CRF, GI ulceration and bleeding are common. Hypertension is present in > 80% of patients with advanced renal insufficiency and is usually related to hypervolemia and occasionally to activation of the renin-angiotensin-aldosterone system. Cardiomyopathy (hypertensive, ischemic) and renal retention of Na and water may lead to congestive heart failure or dependent edema. Pericarditis, usually seen in chronic uremia, may occur in acute, potentially reversible, uremia.

The skin may appear yellow-brown; occasionally, urea from sweat may crystallize on the skin as uremic frost. Pruritus is especially uncomfortable for some patients. Renal osteodystrophy (abnormal bone mineralization resulting from hyperparathyroid function, calcitriol deficiency, elevated serum phosphorus, or low or normal serum Ca) usually takes the form of hyperparathyroid bone disease (osteitis fibrosa). Osteomalacia from chronic exposure to aluminum salts used as phosphate-binders and dialysate contamination was once common but has decreased to about 5% of cases. An increasingly prevalent form of renal osteodystrophy is adynamic bone disease, the predominant bone lesion in peritoneal dialysis (60%); it is nearly as prevalent as osteitis fibrosis (about 36% vs. 38%) in hemodialysis patients.

Abnormalities with lipid metabolism also occur with CRF, on dialysis, and after renal transplantation. The primary finding in CRF and dialysis is hypertriglyceridemia; the total cholesterol level is usually normal.