Renal lesions in chronic pancreatitis.

Many patients with chronic pancreatitis (CP), even in the absence of intrinsic renal disease, are found to have abnormal urine, with persistent proteinuria, cylindruria, microhematuria and leukocyturia. The kidneys of 12 necropsy cases with CP showed mild to moderate arterial and arteriolar nephrosclerosis and no other significant changes. Renal biopsies were performed in 10 patients with CP without evidence of systemic disease or intrinsic renal disease, but with persistent urinary abnormalities. By light microscopy, mild arterial and arteriolar nephrosclerosis was present in 5 instances. In 1 patient, evidence of the reparative phase of acute tubular necrosis was noted. In 5 biopsies, electron microscopy revealed minimal to mild increase in mesangial matrix. Mild thickening of the glomerular basement membrane (GBM) was found in three instances but there was no clear-cut evidence of diabetic glomerulosclerosis. The presence of subendothelial electron-lucent material in 3 cases suggests the possibility of previous subclinical episodes of intravascular coagulation. The most consistent finding was the presence of lipid material in the cytoplasm of glomerular and tubular cells. The renal lesions associated with CP are mild, nonspecific and nonprogressive. Various pathogenetic factors can be invoked to account for their presence and for the urinary abnormalities found in patients with CP.

Bartter's syndrome: an overview.

Bartter's syndrome, which is characterized by hypokalemic hypochloremic alkalosis, renal juxtaglomerular hyperplasia, elevated renin and aldosterone, and normal or low blood pressure, has been ascribed to a variety of etiologies. Most recently, the prostaglandins have been in the forefront of the pathophysiologic discussion. Two cases with appropriate renal biopsies are reviewed, as are the clinicopathologic pathways. It is important that strict criteria be applied, and confirmation by renal biopsy is urged.

Membranous nephropathy: an overview.

Membranous nephropathy (MN) accounts for about 20 percent of cases of the nephrotic syndrome. The importance of renal biopsy in establishing the diagnosis is emphasized. In the great majority of MN patients, no etiologic factor can be discerned. In a significant minority, MN appears to be a manifestation of sarcoidosis, diabetes, lupus, syphilis, malaria, or toxicity from heavy metals or drugs. In some cases the "cause" is neoplasia (including lymphoma) or a viral infection. Massive proteinuria, hypoproteinemia and edema are the principal manifestations of MN, finally resulting in renal failure. Treatment consists chiefly of diet and diuretic drugs. In the more pronounced cases, corticosteroids may have a favorable effect and in very resistant cases, cyclophosphamide is indicated. Judicious use of these modalities if often associated with the diminution or disappearance of the clinical signs of MN.

Membranous glomerulopathy in a patient with sarcoidosis.

We describe a case of membranous nephropathy in a patient with pulmonary, splenic and hepatic sarcoidosis. The patient was asymptomatic, and edema was absent notwithstanding the proteinuria (over 8.0 gm/100 ml daily). Prednisone cleared the pulmonary and splenic complications, but the proteinuria, although diminished, persisted. Adjunctive therapy with cyclophosphamide caused further diminishment of the proteinuria. We have reviewed the relationship between the nephropathy and the sarcoidosis and suggest that a causal relationship exists between the two diseases.