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Improving renal function by treating hypercalcemia

par Tomeba Siwe, Amélie Laure;Taghavi, Maxime ;Casimir, Madeleine ;Fosso, Christelle ;Nechita Mariana, Irina;Collart, Frédéric
Référence 24th Annual Congress of the Belgian Society of Internal Medicine(13–14 December 2019: Dolce La Hulpe, La Hulpe, Belgium), Acta Clinica Belgica, Abstracts presented at the 24th Annual Congress of the Belgian Society of Internal Medicine, Vol. 74, page (56), poster communication 72
Publication Publié, 2019-11-15

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Résumé :

Introduction: Sarcoidosis is a chronic multisystemic inflammatory disorder of unknown etiology. Its diagnosis usually involves weighing the clinical evidence for and against the diagnosis, coupled in most cases with histologic evidence of non-necrotizing granulomatous inflammation. The most common histological finding in renal biopsy is interstitial nephritis with granulomas; however, the latter can be absent. Hypercalcemia and hypercalciuria are a major cause of renal impairment, predisposing to pre-renal azotemia, acute tubular necrosis, nephrolithiasis and nephrocalcinosis.Clinical case: A 54 years old woman with arterial hypertension and diabetes mellitus. She was admitted in the nephrology department for severe hypercalcemia and acute kidney failure in the context of chronic kidney disease. She complained of extreme weakness, vomiting and headache.The blood sample showed: Creatinine:7.02 mg/dL (normal values:0.57-1.11), Urea 116 mg/dL (nv 15-39), Creatinine Clearance eGFR (CKD-EPI): 6 mL/min/1.73m2, Ca: 3.49 mmol/L (nv 2.10-2.55), Ca corrected: 3.51 mmol/L, P:1.94 mmol/L (nv 0.74-1.52), 1.25 di OH-vitamin D: 60,9 μg/ml (nv 25-86), Quantiferon TB Gold was negative. Angiotensin Converting Enzyme: 178 U/L (nv 8-55). Urinalysis showed: calcium: 1,58 mmol/L, Calcium/Creatinine 0.593 mol/mol Creatinine (nv <0.700), Proteins/Creatinine 0.47 g/g Creatinine (nv<0.20). Blood in Traces. Renal ultrasound showed that both kidneys were normal sized, without obstruction or lithiasis. Chest CT and PET Scan confirmed the presence ofmultiple mediastinal and hilar bilateral lymph nodes, multiple micronodules and the absence of pulmonary fibrosis. Abdominal CT showed Microlithiasis around 1 to 2 mm on the inferior chalice of the right kidney. Renal biopsy showed interstitial fibrosis with tubular atrophy and calcium precipitation in the tubules presumably secondary to hypercalcemia. Glomerulosclerosis of probable diabetic origin was noticed. IV fluids and loop diuretics treatment were started. Patient was also prepared for emergency start of peritoneal dialysis with insertion of catheter. A slight but significant improvement in eGFR was observed. By corroborating the clinical, biological and pathological elements (presence of mediastinal and hilar bilateral lymphadenopathy, renal interstitial fibrosis, splenomegaly, non-parathyroid-related hypercalcaemia, calcium urinary lithiasis and elevated ACE levels), we decided to treat this hypercalcemia with renal failure, as due to sarcoidosis, by giving prednisolone 10 mg/day. Significant improvement of renal function (eGFR: from 13 to 19 ml/min/1.73m2) and calcium level (from 3,68 to 2,71 mg/dl) was observed at 6 weeks.Conclusion: Hypercalcemia has been described in patients with granulomatous disorders, most commonly sarcoidosis and tuberculosis. Glucocorticoids are the mainstay of therapy of sarcoidosis even though the ideal dose and duration are not known with certainty, because of lack of data from randomized controlled studies. They are also an indication for the treatment of Hypercalcemia. The difficulty to confirm the diagnosis of sarcoidosis remains, because of the variability of the clinical presentation. Even when the diagnostic is not certain and the renal involvement is not granulomatous, treatment of hypercalcemia is essential to improve the renal function. In our case, the treatment with corticosteroids have improved renal function and hypercalcemia in 6 weeks.