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These drugs decrease proteinuria and consequently the need for albumin infusion. NSAID effect on decreasing proteinuria exceeds a simple decrease in glomerular filtration rate but seems to directly modify renal hemodynamics.[3] ACEi interfere with the reninangiotenisn-aldosteron cascade and reduce proteinuria both in animals and humans.[4] The use of ACEi together with NSAID have been described to decrease but not a complete disappearance of proteinuria as noted here. B. Aoun1,2, C. P. Schmitt3, T. Ulinski4, H. Fakhoury1, G. Kalkas1, S. Sanjad1,2 1 Department of Pediatric Nephrology, Rafic Hariri University Hospital, Beirut, Lebanon, 2Faculty of Medicine, American University of Beirut, 3Center for Pediatric and Adolescent Medicine, University of Heidelberg, Germany, 4Armand Trousseau University Hospital University, Paris, France Address for correspondence: Dr. Bilal Aoun, Department of Pediatric Nephrology, Rafic Hariri University Hospital, Beirut, Lebanon. E‑mail:
[email protected]
References 1.
Tudorache E, Hogan J, Dourthe ME, Quinet B, Grimprel E, SellierLeclerc AL, et al. Congenital nephrotic syndrome with acute renal failure. Pediatr Nephrol 2012;27:47,49-50. 2. Jackson LW. Congenital nephrotic syndrome. Neonatal Netw 2007;26:47‑55. 3. Vriesendorp R, Donker AJ, de Zeeuw D, de Jong PE, van der Hem GK, Brentjens JR. Effects of nonsteroidal anti‑inflammatory drugs on proteinuria. Am J Med 1986;25;81:84‑94. 4. Sreedharan R, Bockenhauer D. Congenital nephrotic syndrome responsive to angiotensin-converting enzyme inhibition. Pediatr Nephrol 2005;20:1340-2. Access this article online Quick Response Code:
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Posterior reversible encephalopathy syndrome in minimal change disease Sir, An 11‑year‑old girl was being treated elsewhere from the age of 5 years for nephrotic syndrome. She received Indian Journal of Nephrology
prednisolone 30 mg per day until remission followed by tapering. She had several relapses during the last 5 years, and presented to us in nephrotic state. Her pulse rate and blood pressure were 78 bpm and 90/70 mmHg, respectively. Systemic examination was unremarkable. Investigations revealed blood urea: 12 mg/dL, serum creatinine: 0.7 mg/dL, serum proteins: 4.7 g/dL, serum albumin: 2.1 g/dL, 24 h urine protein: 4.5 g, serum cholesterol: 450 mg/dL, serum LDL: 267 mg/dL, serum HDL 60 mg/dL, serum VLDL: 158 mg/dL, serum triglycerides 615 mg/dL, hemoglobin: 12 g/dL. Renal biopsy revealed 11 glomeruli, and findings were consistent with minimal change. She received 65 mg of prednisolone in three divided doses per day according to the ISKDC protocol.[1] After 3 weeks, she presented with multiple episodes of generalized tonic clonic seizures. She was afebrile, pulse rate was 160 bpm, blood pressure was 110/60 mmHg. Glasgow coma scale was 7/15. Cerebrospinal fluid analysis revealed 3 cells/hpf, glucose: 56 mg/dL, protein: 15 mg/dL. MRI brain showed bilateral asymmetrical T2, FLAIR hyperintense lesions in cortical and subcortical location of parieto‑occipital, temporal lobes, bilateral thalami, and cerebellum suggestive of posterior reversible encephalopathy syndrome (PRES)[Figure 1]. She was treated with antiepileptics and the dose of prednisolone was reduced to half. She recovered completely in 48 h. PRES, originally termed reversible posterior leukoencephalopathy syndrome [2] presents with headache, seizures, visual changes, altered mental status, and occasionally focal neurologic signs.[3] CT and MR imaging typically show symmetrically distributed areas of vasogenic oedema predominantly within the territories of the posterior circulation.[3] PRES is seen with a heterogeneous group of disorders.[3] In renal disorders, it is reported with hemolytic the uremic syndrome, thrombotic thrombocytopenic purpura, as a complication of Cyclosporine and tacrolimus,[3,4] and acute poststreptococcal nephritis[4] In patients with the nephrotic syndrome, the risk factors are administrationof cyclosporine, tacrolimus, [4] methylprednisolone, [5] hypertension and renal insufficiency. However, nephrotic syndrome itself could be considered a predisposing condition for developing PRES in both adults and children. [6] The key pathophysiological process of PRES is vasogenic edema.[2] due to decreased intravascular oncotic pressure, increased permeability of intracerebral capillaries, and fluid overload. Drugs such March 2012 / Vol 22 / Issue 2
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Figure 1: MRI brain: Posterior reversible encephalopthy syndrome
as cyclosporine, tacrolimus, and methylprednisolone may induce vasogenic oedema by alterating sympathetic flow, cyclosporine‑mediated release of endothelin, or endothelial dysfunction, while hypertension may also induce oedema due to autoregulation failure of the cerebral blood flow. G. Swarnalatha, R. Ram, B. H. S. Pai, K. V. Dakshinamurty Nizam’s Institute of Medical Sciences, Punjagutta, Hyderbad, India Address for correspondence: Dr. K. V. Dakshinamurty, Nizam’s Institute of Medical Sciences, Punjagutta, Hyderabad, India. E‑mail:
[email protected]
References 1.
Report of International Study of Kidney Disease in Children: The primary nephrotic syndrome in children. Identification of patients with minimal change nephrotic syndrome from initial response to prednisone. A report of the International Study of Kidney Disease in Children. J Pediatr 1981;98:561‑4. 2. Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, 154
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et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334:494‑500. 3. Covarrubias DJ, Luetmer PH, Campeau NG. Posterior reversible encephalopathy syndrome: Prognostic utility of quantitative diffusion‑weighted MR images. AJNR Am J Neuroradiol 2002;23:1038‑48 4. Ishikura K, Ikeda M, Hamasaki Y, Hataya H, Shishido S, Asanuma H, et al. Posterior reversible encephalopathy syndrome in children: Its high prevalence and more extensive imaging findings. Am J Kidney Dis 2006;48:231‑8 5. Ikeda M, Ito S, Hataya H, Honda M, Anbo K. Reversible posterior leukoencephalopathy in a patient with minimal‑change nephrotic syndrome. Am J Kidney Dis 2001;37:E30. 6. Pearson ER, D’Souza RJ, Hamilton‑Wood C, Nicholls AJ, Beaman M. Hypertensive encephalopathy and nephrotic syndrome: A possible link? Nephrol Dial Transplant 1999;14:1750‑2.
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