Isoniazid and rifampicin are used for management of tuberculosis. Acute poisoning due to isoniazid overdose is associated with repetitive generalized tonic-clonic seizures and severe metabolic acidosis. In toxic doses, rifampicin is known to produce hepatic, renal, hematological disorders, and convulsions. Sometimes, it may produce red man syndrome. We report a case of fatal poisoning with isoniazid and rifampicin. The case was characterized by late presentation, lactic acidosis, and renal failure.

Distal renal tubular acidosis (dRTA) is an autosomal recessive syndrome results defect in either proximal tubule bicarbonate reabsorption or in distal tubule H(+) secretion and is characterized by severe hyperchloraemic metabolic acidosis in childhood. dRTA is associated with functional variations in the ATP6V1B1 gene encoding β1 subunit of H(+)-ATPase, key membrane transporters for net acid excretion of α-intercalated cells of medullary collecting ducts. In the present study, a 13-year-old male patient suffering with nephropathy and sensorineural deafness was reported in the Department of Nephrology. We predicted improper functioning of ATP6V1B1 gene could be the reason for diseased condition. Therefore, exons 3, 4, and 7 contributing active site of ATP6V1B1 gene was amplified and sequenced (Accession numbers: KF571726, KM222653). The obtained sequences were BLAST searched against the wild type ATP6V1B1 gene which showed novel mutations c.307 A > G, c.308 C > A, c.310 C > G, c.704 T > C, c.705 G > T, c.709 A > G, c.710 A > G, c.714 G > A, c.716 C > A, c.717delC, c.722 C > G, c.728insG, c.741insT, c.753G > C. These mutations resulted in the expression of truncated protein terminating at Lys 209. The mutated ATP6V1B1structure superimposed with wild type showed extensive variations with RMSD 1.336 Å and could not bind to substrate ADP leading to non-functional ATPase. These results conclusively explain these mutations in ATP6V1B1 gene resulted in structural changes causing accumulation of H(+) ions contributing to dRTA with sensorineural deafness.

The reports of glomerular lesions of kidney due to tuberculosis are sparse. A 48-year-old gentleman, presented with swelling of feet of 3 months duration. As he had renal impairment, proteinuria and normal-sized kidneys, he was subjected to renal biopsy. The light microscopy and immunofluorescence revealed the diagnosis was membrano-proliferative glomerulonephritis. During hospital stay, the patient complained fever and stiffness at thoracic spine. The MRI of thoraco-lumbo-sacral spine revealed paravertebral abscess at D11-D12. The pus aspirated was positive for Mycobacterium tuberculosis. He was started on anti-tuberculous medication. After 8 weeks of therapy, the serum creatinine was 1.5 mg/dL and 24 h urine protein 250 mg.Keywords: acid-fast bacilli; membranoproliferative glomerulonephritis; nephrotic syndrome; Pott's disease; Ziehl-Neelsen stain Tuberculous involvement in the genitourinary tract is well reported in literature. However, reports of glomerular lesions due to tuberculosis are sparse. We report a patient with an association of tuberculosis and membranoproliferative glomerulonephritis.A 48-year-old man presented to our institute with complaints of swelling of the feet of 3 months duration. He also had a history of facial puffiness and oliguria. There was no history of haematuria or pyuria. He had no history of passing stones in the urine. There was history of prolonged frothiness of urine. On examination, blood pressure was 140/90 mmHg, he had paedal oedema, and facial puffiness. He had no history of hypertension or diabetes mellitus. Cardiovascular, respiratory and abdomen examinations were unremarkable. Results of other investigations were blood urea, 17.5 mmol/L (50 mg/dL); serum creatinine, 166.2 µmol/L (1.88 mg/dL); serum sodium, 134 mmol/L (134 mEq/L); serum potassium, 3.9 mmol/L (3.9 mEq/L); total serum protein, 60 g/L (6 g/dL); serum albumin, 30 g/L (3 g/dL); haemoglobin, 115 g/dL (11.5 g/ dL); 24-h urine protein, 1400 mg; urine albuminm 3+; red blood cells, 10-12/hpf; white blood cells, 10-12/hpf; ultrasound abdomen, right kidney: 11.3 × 5.1 cm and left kidney 10.2 × 4.8 cm, anti dsDNA, C-ANCA and P-ANCA: negative, C 3: 620 (reference range: 970-1576 mg/L), C 4: 79 (reference range: 102-445 mg/L).As he had renal impairment, proteinuria and normalsized kidneys, he was subjected to renal biopsy. Three linear grey-white soft tissue bits were reported with 10 glomeruli, all of them showing an increase in mesangial cell proliferation and mesangial matrix. There was lobular accentuation in all of them (Figure 1 and Supplementary Figure 1), a few of them showing neutrophil and lymphocyte infiltration. Tubules showed red blood cell casts. There was focal moderate interstitial lymphomononuclear infiltrate. Blood vessels were unremarkable. Immunofluorescence (IF) showed granular deposition of C3 in the capillary walls, outlining the lobular structure of the glomerulus. In addition IgG was also found, but was of less intensity. IgM, IgA, C1q and light chains were absent. The diagnosis was ...

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Gall stone ileus is a rare serious complication of cholelithiasis. We report a case of cholecystoduodenal fistula presenting as gall stone ileus with acute kidney injury which was managed successfully.