Diagnostic and therapeutic strategies in hyperoxaluria: a plea for early intervention

Höppe, Bernd; Leumann, Ernst

doi:10.1093/ndt/gfg507

Cited by 42 publications

(34 citation statements)

References 26 publications

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“…Based on expert opinion, conservative measures should be implemented soon after diagnosis and include a diet low in oxalate and relatively high in calcium, maintenance of high fluid intake (at least 1.5 L per 1.73 m 2 per day) and consideration of potassium citrate to alkalinize urine to increase solubility of oxalate crystals. 13 The role of probiotics is controversial, with studies showing conflicting results.…”

Section: Managementmentioning

confidence: 99%

Oxalate nephropathy from cashew nut intake

Bernardino¹,

Parmar

2016

CMAJ

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Section: Managementmentioning

confidence: 99%

Oxalate nephropathy from cashew nut intake

Bernardino¹,

Parmar

2016

CMAJ

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“…A massive elevation of urinary oxalate excretion results in recurrent kidney stones and/or progressive nephrocalcinosis and often to early end-stage renal disease (ESRD). There is a high clinical heterogeneity of the disease with the infantile form presenting very early with severe bilateral nephrocalcinosis and renal failure usually by the age of 2 years at one end and adult patients with occasional passage of single calculi and preserved renal function at the other end of the spectrum [1][2][3]. With disease progression, even in the stage of mild renal insufficiency, plasma oxalate levels begin to increase and calcium oxalate deposition occurs in various tissues such as bones, heart, thyroid, retina, nerves and blood vessels.…”

Section: Introductionmentioning

confidence: 99%

“…Thus, early diagnosis is of utmost importance to start aggressive medication in order to prevent progression to ESRD. Nevertheless, the treatment armamentarium of patients with PH is limited, consisting of high fluid intake and medication to increase the urinary solubility of calcium oxalate [1][2][3]. Treatment with pyridoxine, the cofactor of the defective AGT enzyme, helps to reduce urinary oxalate excretion only in about a third of patients.…”

Section: Introductionmentioning

confidence: 99%

Late diagnosis of primary hyperoxaluria after failed kidney transplantation

et al. 2009

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Primary hyperoxaluria type 1 (PH1) is a rare autosomal recessive inborn error of the glyoxylate metabolism that is based on absence, deficiency or mislocalization of the liver-specific peroxisomal enzyme alanine:glyoxylate aminotransferase. Hyperoxaluria leads to recurrent formation of calculi and/or nephrocalcinosis and often early end-stage renal disease (ESRD) accompanied by systemic calcium oxalate crystal deposition. In this report, we describe an adult female patient with only one stone passage before development of ESRD. With unknown diagnosis of PH, the patient received an isolated kidney graft and developed an early onset of graft failure. Although initially presumed as an acute rejection, the biopsy revealed calcium oxalate crystals, which then raised a suspicion of primary hyperoxaluria. The diagnosis was later confirmed by hyperoxaluria, elevated plasma oxalate levels and mutation of the AGXT gene, showing the patient to be compound heterozygous for the c.33_34InsC and c.508G > A mutations. Plasma oxalate levels did not decrease after high-dose pyridoxine treatment. Based on this case report, we would recommend in all patients even with a minor history of nephrolithiasis but progression to chronic renal failure to exclude primary hyperoxaluria before isolated kidney transplantation is considered.

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“…- Ox, los cuales promueven la nucleación, crecimiento y agregación de cristales CaOx; una evaluación cuantitativa de la cantidad de estos iones en orina y suero es muy recomendada en animales de compañía con urolitos de CaOx (Leumann y Hoppe, 2001;Milliner, 2005). Adicionalmente, se recomienda evitar el consumo de agua con alto contenido de calcio o pobre en minerales traza como el zinc, que se une al calcio, un monitoreo del DHCC en sangre y reducir la ingesta dietaria , en especial de alimentos ricos en oxalato (Stauffer, 1977).…”

Section: Figura 2 Metabolismo Del Oxalatounclassified

Formación de calculos renales de oxalato cálcico en mamíferos

Neira-Carrillo

Vásquez-Quitral

2012

Avances en Ciencias Veterinarias

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Calcium oxalate (CaOx) is the main inorganic component of urolithiasis and is mainly present in the formation of kidney stones in humans. Additionally, oxalocalcic urolithiasis has become the most frequent type of kidney stones, for instance, oxalocalcic urolithiasis has substantially increased in dogs and cats over the last decades. In urolithiasis, urine is supersaturated with calcium and oxalate ions that promote nucleation, growth and aggregation of CaOx crystals. It is accepted that the presence of acidic macromolecules and inorganic compounds in urine is responsible not only for the molecular processes involved in lithiasis but also for the adhesion and endocytosis by renal epithelial cells. Patients with the tendency to form kidney stones may have an alteration in the structure and/or function of some inhibitors of crystallization. In the current review, we describe some general aspects of epidemiology and pathophysiology of oxalocalcic urolithiasis.

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Diagnostic and therapeutic strategies in hyperoxaluria: a plea for early intervention

Cited by 42 publications

References 26 publications

Oxalate nephropathy from cashew nut intake

Oxalate nephropathy from cashew nut intake

Late diagnosis of primary hyperoxaluria after failed kidney transplantation

Formación de calculos renales de oxalato cálcico en mamíferos

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