CHRONIC KIDNEY DISEASE (CKD) : DIFFERENTIAL DIAGNOSIS AND LABORATORY FINDINGS

Common Causes of Chronic Renal Failure
- Diabetic Nephropathy
- Hypertensive nephrosclerosis
- Glomerulonephritis
- Renovascular disease (ischaemic nephropaty)
- Polycistic kidney disease
- Reflux nephropathy and other congenital renal diseases
- Interstitial nephritis, including analgesic nephropathy
- HIV-associated nephropathy
- Transplant allograft failure

The first step in differential diagnosis of CKD is establishing its chronicity, i.e., disproving a major acute component. The two most common means of determining disease chornicity 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., ther are several relatively common conditions in which kidney disease may be chronic without any reduction in renal disease. Diabetic neuropathy, HIV-associated nephropathy, and infiltrative disease such as multiple myeloma may in fact be associated with relatively large kidneys depite chronicity. Renal biopsy, although rarely performed in patients with CKD, is a more reliable means of proving chronicity, a predominance of glomerulosclerosis or interstitial fibrosis argues strongly for chronic disease. Hyperphosphatemia and other metabolic derangements 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 Hx will identify important comorbid conditions, such as diabetes, HIV Seropositivity or peripheral vascular disease. The family Hx is paramaount in the workup of autosomal dominant polycystic kidney disease or hereditary nephritis (Alport 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 an abdominal bruit (i.e., renovascular disease). The Hx and exam may also yield important data regarding severity of disease. The presence of foreshortened fingers (due to resorption of the distal phalangela tufts) and/or subcutaneous nodules may be seen with advanced CKD and the secondary hyperparathyroidism. Excorations (uremic pruritus), pallor (anemia), muscle wasting, and a nitrogenous fetor are all signs of advanced CKD, as are pericarditis, pleuritis, and aterixis, 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. Heavy proteiunuria (>3,5g/d), hypoalbuminemia, hypercholesterolemia, edema suggest nephritic syndrome. Diabetic nephropathy, membranous nephropathy, focal segmental glomerlusclerosis, minimal change disease, amyloid, and HIV-associated nephropathy are principal causes. Proteinuria may decrease slightly with decreasing GFR but rarely to normal levels. Hyperkalemia and metabolic acidosis may complicate all forms of CKD eventually but can be mor prominent int patiensis with interstitial renal disease.


17th Edition Harrison’s Manual of Medicine

For a more detailed discussion, see Bargman JM, Skorecki K : Chronic Kidney Disease, chap. 274, p.1761, in HPIM-17