{"references": ["1. National Center for Biotechnology Information (US). Genes and Disease. Bethesda (MD): National Center for Biotechnology Information (US); 1998: Alport syndrome.", "2. Kashtan CE. Alport Syndrome. 2001 Aug 28 [Updated 2019 Feb 21]. In: Adam MP, Ardinger HH, Pagon RA, et al, (Eds). GeneReviews. Seattle (WA): University of Washington, Seattle; 1993-2019.", "3. Oni AO, Eweka AO, Otuaga PO, Odia JO. Alport's syndrome . Saudi J Kidney Dis Transp. 2009;20:1087- 9.", "4. Heidet L, Cai Y, Guicharnaud L, Antignac C, Gubler MC. Glomerular expression of type IV collagen chains in normal and X-linkedAlport syndrome kidneys.Am J Pathol. 2000;156(6):1901\u20131910.", "5. Hudson BG. The molecular basis of Goodpasture and Alport syndromes: Beacons for the discovery of the col-lagen IV family. J Am Soc Nephrol 2004;15:2514- 27.", "6. Mukerji N, Dodson K. X-linked Alport syndrome: A case report. Internet J Nephrol. 2003;1:42.", "7. Zhang Y, Ding J: RenalAuricular, and ocular Outcomes of Alport Syndorme and their Current Management. Pediatr Nephrol. 2018;33(8):1309-1316."]}

Alport syndrome is a rare genetic disorder of specialized basement membranes in the kidney, ear, and eye, characterized by haematuria with progressive hereditary nephritis, high-frequency sensorineural hearing loss (SNHL) and pathognomonic ocular lesions. It is one of the spectra of diseases representing hereditary nephritis, which inevitably leads to end-stage renal disease (ESRD). Microscopic or frank haematuria persistent from childhood constitutes the clinical clue for its early recognition. It occurs as a result of genetically inherited or de novo mutations in type IV collagen genes. The most common mode of inheritance is X-linked and men are more severely affected. We report a case of a middle aged man, in his fourth decade of life presenting with persistent haematuria, thrombocytopenia associated with SNHL and anterior lenticonus, diagnosed as a previously undetected case ofAlport syndrome