GLOMERULAR DISEASE



Proteinuria in excess of 0.5 to 1 gm/24 hr is the hallmark of glomerular disease and indicates a functional impairment in the sieving ability of the glomerular capillary with respect to serum mac-romolecules (proteins). The second common sign of glomerular disease consists of cellular ele­ments, red and white blood cells, and cellular casts in the urinary sediment. Sterile pyuria and hematuria with red blood cell (RBC) casts are in­dicators of inflammatory processes. Regardless of the etiology of the glomerular injury, the clinical presentation and course of glomerular diseases converge on the following general patterns.

Nephrosis is a presentation of glomerular injury characterized predominantly by proteinuria with minimal or no cellular sediment in the urine. Ne­phrosis is expressed clinically in edema forma­tion, normal to reduced blood pressure, and nor­mal or slowly decreasing rates of glomerular filtration (GFR). The nephrotic syndrome is a clin­ical syndrome in which heavy proteinuria (usu­ally >3 gm/24 hr) leads to a reduction in the serum albumin (usually <3.0 gm/dl) and is associated with edema formation. Renal salt retention in ne­phrotic glomerulopathies results in expansion of the interstitial compartment of the extracellular fluid volume. Hyperlipidemia and lipiduria are frequent findings in the syndrome.

Nephritis describes a presentation of glomeru­lar injury in which hematuria or a prominent cel­lular urinary sediment occurs along with slight to moderate proteinuria. Hypertension and/or heart failure occur regularly in nephritic glomerulo­pathies because salt retained by the diseased kid­neys results primarily in expansion of the intra­vascular volume. A reduced GFR is usually seen at an early stage in the course of nephritic dis­eases. Focal glomerulonephritis, which affects portions of some glomeruli, may present only with hematuria and proteinuria; the GFR and sys­temic hemodynamic functions may be little af­fected. Diffuse glomerulonephritis, which affects the entirety of most glomeruli, more often pre­sents with clinical signs of ECF volume excess and azotemia in addition to hematuria and pro­teinuria.