Richard A. Matarese

Quantitation of urinary protein excretion is used extensively for diagnostic and prognostic purposes and to assess the effects of therapy. The method most commonly used to measure urinary protein relies on 24-hour urine collections, which are time consuming, cumbersome, and often inaccurate. We reasoned that the urinary protein/creatinine ratio in a single voided urine sample should correlate well with the quantity of protein in timed urine collections. In a study of 46 specimens we found an excellent correlation between the protein content of a 24-hour urine collection and the protein/creatinine ratio in a single urine sample. The best correlation was found when samples were collected after the first voided morning specimen and before bedtime. We conclude that the determination of the protein/creatinine ratio in single urine samples obtained during normal daylight activity, when properly interpreted by taking into consideration the effect of different rates of creatinine excretion, can replace the 24-hour urine collection in the clinical quantitation of proteinuria. In the presence of stable renal function, a protein/creatinine ratio of more than 3.5 (mg/mg) can be taken to represent "nephrotic-range" proteinuria, and a ratio of less than 0.2 is within normal limits.

Non-steroidal anti-inflammatory agents ( NSAIA ) are increasingly used in clinical practice. They exert the majority of their therapeutic and adverse effects by inhibiting prostaglandin synthesis. A variety of clinically important side effects have been described following their administration. We review the renal complications, which include sodium retention, interference with the effectiveness of diuretics, impairment of water excretion, development of hyperkalemia, interference with the therapy of hypertension, and induction of at least four different forms of renal failure. The hemodynamic variety of renal failure and the side effects affecting fluid and electrolyte homeostasis are most likely to become manifest in the context of conditions leading to decreased renal perfusion. Guidelines for use of NSAIA , detection of patients at risk, and therapeutic approaches are provided.

Renal histology of a patient with idiopathic retroperitoneal fibrosis demonstrated a proliferative crescentic glomerulonephritis with intramembranous electron-dense deposits. These findings were interpreted as being consistent with an immune complex glomerulonephritis. Serologic studies revealed a positive antismooth muscle antibody titer of 1:80 and a weakly positive antinuclear antibody titer of 1:40. No distinct systemic disease was identified. While fibrosis of the retroperitoneum can occur in association with a number of distinct pathologic conditions and pharmacologic agents, the mechanism responsible for the development of the idiopathic variety of retroperitoneal fibrosis remains unclear. Our observation of an immune complex glomerulonephritis and the cumulative data on idiopathic retroperitoneal fibrosis are consistent with the concept that the fibrosis may be a local expression of an immunologically mediated systemic disease.