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EPIDEMIOLOGY

The prevalence of chronic kidney disease (CKD), generally defined as a longstanding, irreversible impairment of kidney function, is substantially greater than the number of pts with end-stage renal disease (ESRD), now ≥500,000 in the United States. There is a spectrum of disease related to decrements in renal function; clinical and therapeutic issues differ greatly depending on whether the glomerular filtration rate (GFR) reduction is moderate (stage 3 CKD, 30–59 mL/min per 1.73 m2) (Table 52-1), severe (stage 4 CKD, 15–29 mL/min per 1.73 m2), or "end-stage renal disease" (stage 5 CKD, <15 mL/min per 1.73 m2). Dialysis is usually required once GFR <10 mL/min per 1.73 m2. Common causes of CKD are outlined in Table 149-1.

TABLE 149-1COMMON CAUSES OF CHRONIC RENAL FAILURE

DIFFERENTIAL DIAGNOSIS

The first step in the differential diagnosis of CKD is establishing its chronicity, i.e., disproving a major acute component. The two most common means of determining disease chronicity are the history and prior laboratory data (if available) and the renal ultrasound, which is used to measure kidney size. In general, kidneys that have shrunk (<10–11.5 cm, depending on body size) are more likely affected by chronic disease. While reasonably specific (few false positives), reduced kidney size is only a moderately sensitive marker for CKD, i.e., there are several relatively common conditions in which kidney disease may be chronic without any reduction in renal size. Diabetic nephropathy, HIV-associated nephropathy, and infiltrative diseases such as multiple myeloma may in fact be associated with relatively large kidneys despite chronicity. Renal biopsy, although rarely performed in pts with CKD, is a more reliable means of proving chronicity; a predominance of glomerulosclerosis or interstitial fibrosis argues strongly for chronic disease. Hyperphosphatemia, anemia, and other laboratory abnormalities are not reliable indicators in distinguishing acute from chronic disease.

Once chronicity has been established, clues from the physical exam, laboratory panel, and urine sediment evaluation can be used to determine etiology. A detailed history (Hx) will identify important comorbid conditions, such as diabetes, HIV seropositivity, or peripheral vascular disease. The family Hx is paramount in the workup of autosomal dominant polycystic kidney disease or hereditary nephritis (Alport's syndrome). An occupational Hx may reveal exposure to environmental toxins or culprit drugs (including over-the-counter agents, such as analgesics or Chinese herbs).

Physical exam may demonstrate abdominal masses (i.e., polycystic kidneys), diminished pulses or femoral/carotid bruits (i.e., atherosclerotic peripheral vascular disease), or abdominal or femoral bruits (i.e., renovascular disease). The Hx and exam may also yield important data regarding severity of disease. Excoriations (uremic pruritus), pallor (anemia), muscle wasting, and a nitrogenous fetor are all signs of advanced CKD, as are pericarditis, pleuritis, and asterixis, complications of particular concern that usually prompt the initiation of dialysis.

Laboratory Findings

Serum and urine laboratory findings typically provide additional information useful in determining the etiology and severity of CKD; serial studies determine the pace of progression and/or whether the renal failure is in fact acute. Heavy proteinuria (>3.5 g/d), hypoalbuminemia, hypercholesterolemia, and edema suggest nephrotic syndrome (Chap. 152). Diabetic nephropathy, membranous nephropathy, focal segmental glomerulosclerosis, minimal change disease, amyloid, and HIV-associated ...

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