Medical renal diseases are those that involve principally the parenchyma of the kidneys. Hematuria, proteinuria, pyuria, oliguria, polyuria, pain, renal insufficiency with azotemia, acidosis, anemia, electrolyte abnormalities, and hypertension may occur in a wide variety of disorders affecting any portion of the parenchyma of the kidney, the blood vessels, or the excretory tract.
A complete medical history and physical examination, a thorough examination of the urine, and blood and urine chemistry examinations as indicated are essential initial steps in the workup of any patient.
The family history may reveal disease of genetic origin, for example, tubular metabolic anomalies, polycystic kidneys, unusual types of nephritis, or vascular or coagulation defects that may be essential clues to the diagnosis. First-degree relatives of patients with diabetic renal disease have an enhanced risk of end-stage renal disease, inherited independently of diabetes mellitus.
The past personal history should cover infections, injuries, and exposure to toxic agents, anticoagulants, or drugs that may produce toxic or sensitivity reactions. A history of diabetes, hypertensive disease, or autoimmune disease may be obtained. The inquiry may also elicit symptoms of uremia, debilitation, and the vascular complications of chronic renal disease, but often, the patient is asymptomatic and the diagnosis of renal disease is made incidentally on abnormal laboratory findings.
Pallor, edema, hypertension, retinopathy (either hypertensive or diabetic changes), or stigmas of congenital and hereditary disease may be detected.
Examination of the urine is the essential part of any investigation of renal disease.
Proteinuria of any significant degree (2–4+) is suggestive of medical renal disease (parenchymal involvement). Formed elements present in the urine additionally establish the diagnosis. Significant proteinuria occurs in immune-mediated glomerular diseases or disorders with glomerular involvement such as diabetes mellitus, myeloma, or amyloidosis. Interstitial nephritis, polycystic kidneys, and other tubular disorders are not usually associated with significant proteinuria. To better quantify the degree of proteinuria, one could either collect a 24-hour urine sample or use a spot urine protein to creatinine ratio (measured in milligrams of protein/mg creatinine) as a surrogate (see Figure 33–1).
This graph illustrates the relation between total 24-hour urinary protein excretion and the total protein-to-creatinine ratio (mg/mg) determined on a random urine specimen. Although there appears to be a close correlation, there can be wide variability in 24-hour protein excretion at a given total protein-to-creatinine ratio. At a ratio of 2, for example, 24-hour protein excretion varied from 2 to almost 8 g/d. (Data from Ginsberg JM et al: N Engl J Med 1983;309:1543.)