A 78-year old patient with a history of hypertension and atherosclerosis was referred to our hospital for non-oliguric acute renal failure (ARF). At admission, clinical examination and blood pressure were normal. Laboratory data showed severe renal failure and hypercalcemia (see Table 1). Urine examination was not remarkable. CRP and ESR were normal. Immunological blood tests were negative. Bence Jones proteinuria was negative and serum free light chains in normal range. Normal levels of angiotensin converting enzyme excluded sarcoidosis. On ultrasound, both kidneys were normo-echoic and normal in size; at doppler-ultrasound, renal arteries stenosis were excluded. Thus, renal biopsy was performed.
On light microscopy, 4/9 glomeruli were completely sclerotic, the remnants were normal. Tubular damage was remarkable. Diffuse tubular atrophy, severe acute tubular necrosis, tubulitis, interstitial inflammation with a giant cell reactions around calcium micro-deposits simulating granulomatosus reactions were seen. We also found severe aterosclerosis and moderate arteriolar hyalinosis.
At immunofluorescence, there were granular C3 deposits on vascular polus, Bowman’s capsula and tubules. Electronic microscopy confirmed severe tubular damage with signs of intersitial and tubular inflammation.
On the basis of clinical history and renal biopsy, we made diagnosis of acute renale failure secondary to acute tubular necrosis in patient with idiopathic hypocalciuric hypercalcemia (Hanibuchi N – 2002  (full text)). The patient was treated with hydration, diuretics and a short course of sodium clodronate. At a 12-month follow-up, the patient was on only furosemide therapy; serum creatinine was 3.5 mg/dl and serum calcium in normal range.