Reversible Chronic Interstitial Nephritis Induced by Tacrolimus —Tacrolimus Chronic Interstitial Nephritis

Calcineurin inhibitors (CNI) are potent immunosuppressive agents in prophylaxis against graft rejection and autoimmune diseases including primary glomerulopathies. Previous research showed reversible;acute afferent arteriolar vasculopathy and irreversible chronic interstitial fibrosis associated with CNI nephrotoxicity. In this case report we describe a patient, with minimal change disease, that had developed chronic and progressive renal disease while receiving therapeutic dose of Tacrolimus. His serum creatinine had reached 537 umol/L and his nephrotic state worsened. Kidney biopsy showed chronic interstitial nephritis. Tacrolimus was discontinued and he was treated with 1 mg/kg prednisone in addition to Mycophenolate mofetil (MMF) 1 g twice daily. By the 2nd month;serum creatinine returned to normal and by the 3rd month serum albumin too. After 1 month of therapy;the dose of Prednisone was tapered down gradually till 5 mg daily by the end of 3rd month. Moreover, the dose of MMF was reduced to 500 mg X2 by the end of 3rd month. After 2 years of follow up;he remained stable and without relapse of NS or renal failure. In conclusion, reversible renal disease, due to chronic interstitial nephritis can be induced by CNI which is amenable to treatment with Prednisone and MMF.

A Case of Staphylococcus Associated Glomerulonephritis Confused with Acute Interstitial Nephritis

Staphylococcus associated glomerulonephritis (SAGN) is an uncommon infection-related glomerulonephritis. Although infection is typically ongoing when patients present with SAGN, in the case of deep-seated infections, the presence of infection may not be apparent. The aim of this study is to highlight the importance of renal biopsy when the diagnosis is not obvious. We present a case of staphylococcus associated glomerulonephritis in a patient treated with beta-lactam antibiotics for staphylococcus bacteraemia. A renal biopsy helped differentiate between interstitial nephritis and staphylococcus associated glomerulonephritis.

Severe acute kidney injury due to oxalate crystal induced severe interstitial nephritis:A case report

BACKGROUND Acute kidney injury(AKI)due to interstitial nephritis is a known condition primarily attributed to various medications.While medication-induced interstitial nephritis is common,occurrences due to non-pharmacological factors are rare.This report presents a case of severe AKI triggered by intratubular oxalate crystal deposition,leading to interstitial nephritis.The aim is to outline the case and its management,emphasizing the significance of recognizing uncommon causes of interstitial nephritis.CASE SUMMARY A 71-year-old female presented with stroke-like symptoms,including weakness,speech difficulties,and cognitive impairment.Chronic hypertension had been managed with hydrochlorothiazide(HCTZ)for over two decades.Upon admis-sion,severe hypokalemia and AKI were noted,prompting discontinuation of HCTZ and initiation of prednisolone for acute interstitial nephritis.Further investigations,including kidney biopsy,confirmed severe acute interstitial nephritis with oxalate crystal deposits as the underlying cause.Despite treatment,initial renal function showed minimal improvement.However,with prednisolone therapy and supportive measures,her condition gradually improved,high-lighting the importance of comprehensive management.CONCLUSION This case underscores the importance of a thorough diagnostic approach in identifying and addressing uncommon causes of interstitial nephritis.The occurrence of interstitial nephritis due to oxalate crystal deposition,especially without typical risk factors,emphasizes the need for vigilance in clinical practice.

Epidemiological, Clinical and Follow-Up Data in a Series of Thirteen Renal Insufficiencies Complicating Sarcoidosis

The sarcoidosis is a systemic granulomatosis affecting most frequently the lungs and the mediastinum. An acute renal failure reveals exceptionally this disease. It’s a retrospective study implicating 13 cases of sarcoidosis complicated of acute renal failure. The aim of this study is to determine epidemiological, clinical, biological and histological profile in these cases and the interest of considering sarcoidosis diagnosis in case of unexplained renal failure. Extra-renal complications, therapeutic modalities and the outcome were determined in all patients. Our series involved 13 women with an average age of 41 years. Biological investigations showed an abnormal normocalcemia in 8 cases, a hypercalcemia in 5 cases, a hypercalciuria in 11 cases and polyclonal hypergammaglobulinemia in 7 cases. An acute renal failure was found in all patients with a median creatinin of 540 umol/L. The renal echography was normal in all patients. The kidney biopsy performed in all patients showed tubulo-interstitial nephritis. The extra-renal signs were: pulmonary interstitial syndrome in 5 cases, a sicca syndrome in 4 cases, mediastinal lymphadenopathy in 2 cases, a lymphocytic alveolitis in 3 cases, an anterior granulomatous uveitis in 3 cases and a polyarthritis in 6 cases. Six patients benefited from hemodialysis. The treatment consisted of corticosteroid in all cases. The follow up was marked by complete resolution of clinical and biological signs. The diagnosis of renal sarcoidosis should be made rapidly in order to avoid end stage renal failure.

Hypokalemic Paresis Revealing a Primary Sjogren’s Syndrome

Hypokalemic acidosis can complicate a primary Sjögren’s syndrome. The clinical feature is rarely revealed by manifestations due to hypokalemia. We report the case of a 46-year-old woman, admitted to explore a paresthesia and paresis of inferior limbs. The diagnosis of Sjögren’s syndrome was retained since there was the association of xerophthalmia, sialadenitis at the labial biopsy and positive immunological results (anti-SSA and anti-SSB). The absence of another auto-immune or systemic illness allowed us to consider that the Sjögren’s syndrome was primary. The biological explorations revealed a hyperchloremic and hypokalemic acidosis. The treatment was based on corticosteroid and potassium supplementation. The follow-up was marked by a clinical and biological amelioration.