A 58‐year‐old man presented with progressively worsening bilateral lower‐extremity edema over a 3‐week period. He noted that he had left lower‐extremity edema for the past 2.5 yers but in the past 3 weeks his edema migrated to both legs and moved up to his midthigh. He also noted a weight gain of 10–15 pounds over the past 3 weeks. This weight gain was accompanied by dark urine with no hematuria and shortness of breath for 3 days. He denied any chest pain. He was recently diagnosed with hepatitis C and a deep vein thrombosis of the lower extremity of unknown cause. He denied any current intravenous (IV) drug use, but admitted to a remote use of IV heroin as a teenager. His abdomen was distended and nontender, with no organomegaly noted. Pitting edema was seen in his lower extremities through his thighs as well as abdominal and scrotal edema. He had mild bibasilar crackles and normal cardiac exam. Computed tomography (CT) of the chest and abdomen showed cardiomegaly, pulmonary vascular congestion and a normal liver, kidneys, and spleen. Laboratory studies revealed a BUN/creatinine ratio of 36/2.0, urine protein/urine creatinine ratio of 10.9, AST of 45, ALT of 78, and hypocomplementemia. Glomeruli biopsy revealed granular IgM along the capillary loops and granular C3 along the glomerular capillary basement membrane. At that time, he was diagnosed with membranoproliferative glomerulonephritis (MPGN) secondary to hepatitis C.
Progressive edema is a common clinical presentation to the hospitalist. Although it has a number of causes, renal dysfunction in general and MPGN specifically should be on the differential diagnosis for any hospitalist facing these symptoms. In this patient and with MPGN, immune complexes in the glomeruli have deposited secondary to persistent antigenemia. In this case, the persistent antigenemia resulted from hepatitis C infection. It also resulted in the activation of the classical pathway of complement and the deposition of those factors in the glomeruli. Hepatitis C is a common infectious cause of MPGN, but any form of chronic infection can theoretically cause this disease process.
As it was noted that the patient had diffuse edema and proteinuria, renal causes of edema became the focus of this investigation, and cardiac or hepatic causes became lower on the differential diagnosis. After the patient's profound proteinuria, negative cryoglobulinemia and hypocomplimentemia was noted, and the renal biopsy confirmed the diagnosis of immune complex‐mediated membranoproliferative glomerulonephritis. Tying in the pathophysiology of 2 diseases, membranoproliferative glomerulonephritis is a treatable and intellectually stimulating disease that should be on the differential of any general internist.
To cite this abstract:Al‐Dujaili L. Mpgn: A Treatable and Serious Cause of Nephrotic Syndrome. Abstract published at Hospital Medicine 2013, May 16-19, National Harbor, Md. Abstract 245. Journal of Hospital Medicine. 2013; 8 (suppl 2). https://www.shmabstracts.com/abstract/mpgn-a-treatable-and-serious-cause-of-nephrotic-syndrome/. Accessed May 24, 2019.