Hypercalciuria may predict better response to immunosuppressive therapy in renal sarcoidosis: a case series

Renal sarcoidosis is a rare cause of tubulointerstitial nephritits (TIN). The clinical and pathological characteristics, as well as outcomes, of renal sarcoidosis remain unclear.

This single-center study retrospectively analyzed 18 patients affected by sarcoidosis with tubulointerstitial nephritis (TIN) and 53 patients with tubulointerstitial nephritis  not related to sarcoidosis. Patients were further stratified into the granulomatous (12 sarcoidosis and 6 non-sarcoidosis) and non-granulomatous (6 sarcoidosis and 47 non-sarcoidosis) TIN groups.

Half of the patients with renal sarcoidosis had signs of acute kidney injury at kidney biopsy, 94% of whom presented with extra-renal involvement. The prevalence of hypercalcemia, hypercalciuria, and elevated serum angiotensin-converting enzyme levels was 27.6%, 33.3%, and 31.3%, respectively. Renal sarcoidosis patients with eGFR < 30 mL/min/1.73 m² scored higher for total chronic tubulointerstitial injury (p = 0.044) and glomerular sclerosis (p = 0.027). Compared to non-sarcoidosis patients, higher urinary calcium levels (for patients with GFR \(\ge\) 40 mL/min/1.73 m², p = 0.034), lower scores of acute tubular injury (p = 0.008), and more prominent glomerular sclerosis were observed in renal sarcoidosis. Similar characteristics of chronicity and hypercalciuria were also identified in granulomatous interstitial nephritis; however, interstitial inflammation was obvious (p = 0.001). Patients with renal sarcoidosis were initially treated with corticosteroids. Five patients receiving immunosuppressive agents showed better long-term renal recovery. High 24-h urine calcium (adjusted by weight) was identified as a factor associated with long-term remission.

Renal sarcoidosis is a systemic disease of insidious onset and chronic progression, sharing similar features of chronicity and hypercalciuria with granulomatous interstitial nephritis of other cause. Hypercalciuria may predict a better response to immunosuppressive therapy, presumably indicating active interstitial inflammation; thus, strengthened immunosuppression might be considered.