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Sarcoidosis-associated renal manifestations range from disordered calcium metabolism with nephrolithiasis, to tubulointerstitial nephritis with or without granulomatous infiltration, and rarely glomerular disease, such as membranous nephropathy, focal segmental glomerulosclerosis, IgA nephropathy, and crescentic glomerulonephritis. Renal dysfunction from other co-morbidities must also be considered. We present two cases of biopsy-proven secondary IgA nephropathy from sarcoidosis.
A 42-year-old man experienced new-onset dysphagia, weight loss, and night sweats. Initial imaging revealed mediastinal and periportal lymphadenopathy, splenomegaly, and normal kidney structure. Oncologic workup with bone marrow biopsy was normal. Patient developed progressively worsening symptoms with acute kidney injury (AKI), (serum creatinine (SCr) 3.03 mg/dL) and proteinuria (UPCR 0.217 mg/mg; UA 8 months prior: 1+ blood and 2+ protein). Lymph node biopsy showed non-caseating granulomas and kidney biopsy showed interstitial granulomatous nephritis with 15% IFTA, mesangial expansion with 3+ IgA staining (Oxford M1, E1, S0, T1, C0). Systemic steroids improved renal function and symptoms, were later changed to mycophenolate mofetil due to steroid-myopathy, and dapagliflozin was added for CKD prevention.
A 63-year-old man with hypertension and diabetes mellitus type 2, presented with fatigue and weight loss with AKI (SCr 3.3 mg/dL), hypercalcemia (13.8 mg/dL) with suppressed PTH (9 pg/mL). Urine showed no hematuria, 1+ protein on UA, 544 mg/24 hour. A CT showed non-obstructing 9 mm calyceal stone in the right kidney and PET scan showed lymphadenopathy with lytic bone lesions. Kidney biopsy showed diabetic nephropathy, mild to moderate interstitial fibrosis and inflammation without granulomas, 2+ diffuse IgA staining (Oxford M0, E0, S1, T1, C0) and calcium phosphate deposits. Lymph node biopsy showed non-caseating granulomas and labs showed elevated vitamin D 1,25-OH, ACE and IL2 levels. Systemic steroids were eventually switched to maintenance azathioprine and adalimumab with resolution of hypercalcemia and stabilization of renal function. Given the diabetic nephropathy, empagliflozin and valsartan were initiated.
Secondary IgA Nephropathy has been documented in patients with various comorbidities, including neoplasms, chronic liver disease, viral and other infections, autoimmune conditions and chronic inflammatory states. While the exact pathogenesis of IgA nephropathy coincident with sarcoidosis is unknown, some theories include higher circulation of IgA immune complexes with impaired immunoregulation. The focus of treatment of secondary IgA Nephropathy is directed to the primary process.
In our case, both patients had a favorable response to steroids and were later switched to steroid-sparing immunosuppression to mitigate unfavorable side effects. The use of non-immunologic treatment including RAS blockade and SGLT2i should be considered to mitigate future loss of kidney function, particularly in those with other signs of biopsy-proven kidney disease.
