Journal Information
Vol. 30. Issue. 6.November 2010
Pages 599-714
Vol. 30. Issue. 6.November 2010
Pages 599-714
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Kidney failure and diabetis. Diagnostic inertia?
Insuficiencia renal y diabetes. ¿Inercia diagnóstica?
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R.. Blanco Garcíaa, J.J.. Bravo Lópezb, A.. Pérezc, M.. Moreiras Plazaa
a Servicio de Nefrología, Hospital Xeral, Vigo,
b Servicio de Nefrología, Complexo Hospitalario, Ourense
c Servicio de Anatomía Patológica, Hospital Xeral, Vigo,
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To the Editor,

Diabetes mellitus (DM) is a common cause of kidney failure (KF), but this pathology is not the only aetiology in diabetic patients presenting with renal failure.

We present the case of a 62 year old man with a history of arterial hypertension (AHT), duodenal ulcer, acute myocardial infarction (AMI) and type 2 DM, diagnosed in 2007.

In February 2008, he was admitted to the internal medicine department with pyelonephritis with acute KF (MDRD 21 ml/min), which were interpreted in the context of the infection which was made worse by taking non-steroidal anti-inflammatory drugs (NSAIDs), and continued on discharge. In September 2008, he was referred to the nephrology department presenting with grade 4 KF (MDRD 13.83 ml/min), proteinuria of 5 g/24 h, and persistent microhematuria (negative urine cultures and negative cytology for malignancy). Of note in the rest of the analysis were: Negative ANA, ANCA, and Anti-GBM. Immunoglobulins, light chains, complements, and proteinogram were normal. Blood cultures for HCV, HBV, and HIV were negative. Abdominal ultrasound: kidneys of normal size with moderately cortical echogenicity with no evidence of dilation of the excretory tract. Normal ocular fundus.

In view of the rapid evolution of the KF, without a clear aetiology being known, a kidney biopsy was performed which revealed 21 glomeruli, 6 of them sclerotic and the rest with glomerular mesangial expansion. A crescent formation was observed in one of these. Thickening of the tubular basal membrane and moderate interstitial inflammatory infiltrates was seen, with a predominance of plasma cells, polymorphonuclear neutrophils, and lymphocytes. Immunofluorescence was negative. An electronic microscope showed diffuse thickening of the glomerular basal membrane with the presence of subepithelial electron-dense deposits forming the typical humps (Figure 1).

This finding lead to a diagnosis of post-infectious glomerulonephritis (PIGN) complicating a nephropathy.

Figure 1. E.M: Postinfectious GN. Presence of subepithelial electron-dense deposits (humps)

Bibliography
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Pham TT, Sim JJ, Kujubu DA, et al. Prevalence of nondiabetic renal disease in diabetic patients. Am J Nephrol 2007;27:322. [Pubmed]
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2. Fingerhut D. KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for Diabetes and Chronic Kidney Disease. Am J Kidney Dis 2007;49(Suppl 2). [Pubmed]
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Coppo R, Gianoglio B, Porcellini MG, Maringhini S. Frequency of renal diseases and clinical indications for renal biopsy in children (report of the Italian National Registry of Renal Biopsies in Children). Group of Renal Immunopathology of the Italian Society of Pediatric Nephrology and Group of Renal Immunopathology of the Italian Society of Nephrology. Nephrol Dial Transplant 1998;13:293. [Pubmed]
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Haas M. Incidental healed postinfectious glomerulonephritis: a study of 1012 renal biopsy specimens examined by electron microscopy. Hum Pathol 2003;34(1):3-10. [Pubmed]
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Nasr SH, Markowitz GS, Stokes MB, Said SM, Valeri AM, D¿Agati VD. Acute postinfectious glomerulonephritis in the modern era: experience with 86 adults and review of the literature. Medicine (Baltimore) 2008;87(1):21-32.
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