Case Presentation: The patient was a 23 year old African American male with obesity who presented to the hospital with bilateral lower leg swelling for 2 weeks. He initially noticed the swelling after a 3 hour drive and it resolved after rest and a hot bath. During this time, the patient also noticed increased urinary frequency, foamy urine, and nocturia. This prompted a visit to an urgent care center where he had labs drawn and was told that because of protein in his urine and a high creatinine, he needed to visit the ED. On further questioning, he endorsed having a runny nose 2 weeks prior to his presentation. He denied fevers, cough, chest pain, abdominal pain, hematuria, dysuria, rashes, joint pains, sick contacts, or recent travel. The patient had no previous medical or surgical history, and denied any family history including any history of kidney disease. He denied IV drug use or sexually transmitted diseases. He had not seen a physician in several years. On presentation to the hospital, his vital signs were within normal limits and his physical exam was pertinent for obesity as well as 2+ pitting edema in the lower extremities up to the thighs bilaterally. Pertinent labs included a serum creatinine of 2.31, total protein 5.7, albumin 2.0, ALT 106, and LDL of 351. His UA was positive for >600 protein and he had a negative venous duplex study. The working diagnosis was nephrotic syndrome, but without a clear etiology. He then had an extensive viral and autoimmune workup and was positive for both coronavirus and parvovirus. A kidney biopsy showed collapsing glomerulopathy. The patient was treated with 5 days of IVIG and diuretics with some improvement in his lower extremity edema with a plan for a prolonged course of steroids dictated by nephrology as an outpatient.
Discussion: Collapsing glomerulopathy, also known as collapsing focal segmental glomerulosclerosis, is a disease that is usually seen in African Americans and is often associated with HIV. It has been associated with other viral infections such as CMV and parvovirus, autoimmune, and hematological diseases. It usually presents in middle aged people and often with nephrotic syndrome and rapidly progressive renal failure. The optimal treatment is unknown. The patient in this case, while African American and found to have parvovirus later on, did not have a medical history or the age that one would expect for this extent of kidney disease. The rapid onset of symptoms however and the severity of kidney disease were clues that a more aggressive entity was responsible for the presentation. As a hospitalist, it is important to recognize that not all of the “classic” symptoms associated with a disease may be present in an individual and more rare disorders should be considered when an alternative explanation is not available.
Conclusions: This case serves a reminder that a nephrotic syndrome presentation in a young adult with new onset renal failure may be secondary to a more extensive kidney disease like collapsing glomerulopathy, which can be associated with parvovirus and should be considered by hospitalists even when the typical risk factors are missing.