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1.
J Bras Nefrol ; 46(1): 99-106, 2024.
Artículo en Inglés, Portugués | MEDLINE | ID: mdl-38427579

RESUMEN

We present a case of a 69-year-old man who presented for routine check-up and was incidentally found to have kidney failure with an initially unrevealing history and bland urinary sediment. He was diagnosed with oxalate nephropathy in the setting of chronic turmeric supplementation and chronic antibiotic therapy with associated diarrhea. Our case provides several key insights into oxalate nephropathy. First, the diagnosis requires a high index of clinical suspicion. It is uncommonly suspected clinically unless there is an obvious clue in the history such as Roux-en-Y gastric bypass or ethylene glycol poisoning. Diagnosis can be confirmed by histopathologic findings and corroborated by serum levels of oxalate and 24-hour urinary excretion. Second, the diagnosis can often be missed by the pathologist because of the characteristics of the crystals unless the renal pathologist has made it a rule to examine routinely all H&E sections under polarized light. This must be done on H&E, as the other stains dissolve the crystals. Third, one oxalate crystal in a routine needle biopsy is considered pathologic and potentially contributing to the AKI or to the CKD in an important way. Fourth, secondary oxalosis can be largely mitigated or prevented in many cases, especially iatrogenic cases. This can come through the surgeon or the gastroenterologist providing proper instructions to patients on an oxalate-restricted diet or other specific dietary measures. Lastly, this case highlights the success that results from cooperation and communication between the pathologist and the treating physician.


Asunto(s)
Hiperoxaluria , Insuficiencia Renal , Masculino , Humanos , Anciano , Curcuma , Hiperoxaluria/inducido químicamente , Hiperoxaluria/complicaciones , Insuficiencia Renal/complicaciones , Oxalatos , Suplementos Dietéticos/efectos adversos
2.
BMJ Case Rep ; 12(12)2019 Dec 05.
Artículo en Inglés | MEDLINE | ID: mdl-31811106

RESUMEN

Acute oxalate nephropathy has been associated with chronic diarrheal illness and only one case has been reported due to acute diarrhea secondary to Clostridium difficile colitis. To the best of our knowledge, this is the second case report of acute oxalate nephropathy due to C . difficile colitis. A 75-year-old man with a medical history of hypertension, type 2 diabetes mellitus, chronic kidney disease stage IV, recent C . difficile colitis was admitted for acute kidney injury with a creatinine (Cr) of 8.54 mg/dL (baseline Cr, 2.3-2.6 mg/dL). His urinalysis did not show any eosinophils, casts or crystals. Antinuclear antibody, antineutrophil cytoplasmic antibody, complement levels (C3 and C4) and hepatitis screen were negative; a renal ultrasound visualized no hydronephrosis. A kidney biopsy showed widespread tubular oxalate crystal deposition suggestive of hyperoxaluria as the cause of acute kidney injury. In conclusion, an acute diarrheal illness like C . difficile colitis can cause acute oxalate nephropathy.


Asunto(s)
Lesión Renal Aguda/diagnóstico , Clostridioides difficile/aislamiento & purificación , Enterocolitis Seudomembranosa/diagnóstico , Hiperoxaluria/diagnóstico , Lesión Renal Aguda/complicaciones , Lesión Renal Aguda/patología , Lesión Renal Aguda/terapia , Anciano , Antiinfecciosos/uso terapéutico , Diabetes Mellitus Tipo 2 , Diagnóstico Diferencial , Enterocolitis Seudomembranosa/complicaciones , Enterocolitis Seudomembranosa/tratamiento farmacológico , Enterocolitis Seudomembranosa/microbiología , Humanos , Hiperoxaluria/complicaciones , Hiperoxaluria/terapia , Hipertensión , Masculino , Oxalatos/análisis , Diálisis Renal
3.
J. bras. nefrol ; 46(1): 99-106, Mar. 2024. tab, graf
Artículo en Inglés | LILACS-Express | LILACS | ID: biblio-1534777

RESUMEN

ABSTRACT We present a case of a 69-year-old man who presented for routine check-up and was incidentally found to have kidney failure with an initially unrevealing history and bland urinary sediment. He was diagnosed with oxalate nephropathy in the setting of chronic turmeric supplementation and chronic antibiotic therapy with associated diarrhea. Our case provides several key insights into oxalate nephropathy. First, the diagnosis requires a high index of clinical suspicion. It is uncommonly suspected clinically unless there is an obvious clue in the history such as Roux-en-Y gastric bypass or ethylene glycol poisoning. Diagnosis can be confirmed by histopathologic findings and corroborated by serum levels of oxalate and 24-hour urinary excretion. Second, the diagnosis can often be missed by the pathologist because of the characteristics of the crystals unless the renal pathologist has made it a rule to examine routinely all H&E sections under polarized light. This must be done on H&E, as the other stains dissolve the crystals. Third, one oxalate crystal in a routine needle biopsy is considered pathologic and potentially contributing to the AKI or to the CKD in an important way. Fourth, secondary oxalosis can be largely mitigated or prevented in many cases, especially iatrogenic cases. This can come through the surgeon or the gastroenterologist providing proper instructions to patients on an oxalate-restricted diet or other specific dietary measures. Lastly, this case highlights the success that results from cooperation and communication between the pathologist and the treating physician.


RESUMO Relatamos o caso de um homem de 69 anos que se apresentou para exame de rotina e descobriu-se incidentalmente que ele tinha insuficiência renal, com histórico inicialmente não revelador e sedimento urinário brando. Ele foi diagnosticado com nefropatia por oxalato no contexto de suplementação crônica de cúrcuma e antibioticoterapia crônica com diarreia associada. Nosso caso fornece diversas sugestões importantes sobre nefropatia por oxalato. Primeiro, o diagnóstico requer elevado índice de suspeita clínica. A suspeita clínica é incomum, a menos que haja evidência óbvia no histórico, como bypass gástrico em Y de Roux ou envenenamento por etilenoglicol. O diagnóstico pode ser confirmado por achados histopatológicos e corroborado por níveis séricos de oxalato e excreção urinária de 24 horas. Segundo, o diagnóstico pode passar despercebido pelo patologista devido às características dos cristais, a menos que o patologista renal estabeleça como regra examinar rotineiramente todas as seções coradas com H&E sob luz polarizada. Isso deve ser feito com H&E, pois, outras colorações dissolvem os cristais. Em terceiro lugar, um cristal de oxalato em biópsia por agulha de rotina é considerado patológico, contribuindo potencialmente para LRA ou para DRC de maneira significativa. Em quarto lugar, a oxalose secundária pode ser amplamente mitigada ou prevenida em muitos casos, especialmente casos iatrogênicos. Isso pode ser feito pelo cirurgião ou pelo gastroenterologista, fornecendo instruções adequadas aos pacientes sobre uma dieta restrita em oxalato ou outras medidas dietéticas específicas. Por fim, esse caso destaca o sucesso que resulta da cooperação e comunicação entre o patologista e o médico assistente.

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