Methylene blue induced methemoglobinemia with acute kidney injury in a glucose-6-phosphate dehydrogenase-deficient patient

Our case was treated with methylene blue for symptomatic nitrobenzene poisoning. After which he developed methemoglobinemia with acute kidney injury due to hemolysis and on further testing, he was found to be glucose-6-phosphate dehydrogenase (G6PD) enzyme deficient. Thus, afterward, the patient was treated with only available mode of treatment as repeated blood transfusions and ascorbic acid with dialysis support to which the patient responded. Thus, it is important to evaluate for the G6PD deficiency where methylene blue treatment is planned as an antidote to nitrobenzene compounds poisoning

An uncommon cause of rapidly progressive renal failure in a lupus patient: Pauci-immune crescentic glomerulonephritis

We report a case of systemic lupus erythematosus (SLE) who presented with rapidly progressive renal failure (RPRF) with positive antinuclear antibody (ANA) and anti-double-stranded DNA (dsDNA) antibody and active urinary sediment in the form of microscopic hematuria and proteinuria. Provisional clinical diagnosis of lupus nephritis was made. Renal biopsy showed pauci-immune crescentic glomerulonephritis, the diagnosis of which was supported by positive serum anti-MPO antibody. Renal biopsy in SLE patients can sometimes reveal varied pathological entities such as antinuclear cytoplasmic antibodies (ANCAs) positive vasculitis, as in our case, which modified our treatment protocol. Thus, in a patient with SLE presenting with RPRF with active urinary sediments, ANCA serology, and renal biopsy with immunofluorescence examination should be performed always

Minimal change disease and Kimura's disease responding to tacrolimus therapy

Kimura's disease (KD) usually presents with a subcutaneous swelling and associated lymphadenopathy in the periauricular area. KD has a tendency to involve the kidneys. Proteinuria is reported in 12%–16% of cases, and around 60%–70% of them develop nephrotic range proteinuria. We are reporting a case of KD which developed around 12 years later in a patient of biopsy-proven steroid responsive minimal change disease. Recurrent swellings of KD and subnephrotic range proteinuria responded to low-dose tacrolimus therapy (0.05 mg/kg)

An initial evaluation of hypokalemia turned out distal renal tubular acidosis secondary to parathyroid adenoma

Primary hyperparathyroidism (PHPT) usually presents with hypercalcemia related symptoms and signs. Kidneys play an important role in calcium homeostasis. PHPT has been reported to be associated with hyperchloremia, defective urinary acidification, and renal tubular acidosis (RTA). The dysfunction of distal renal tubules is proposed to be secondary to calcium deposition in distal tubules. This case report highlights an initial presentation of parathyroid adenoma as hypokalemia due to distal RTA secondary to medullary nephrocalcinosis