Secondary Oxalate Nephropathy: A Systematic Review

Abstract

IntroductionLittle is known of the clinical outcomes of secondary oxalate nephropathy. To inform clinical practice, we performed a systematic review of case reports and case series to examine the clinical characteristics and outcomes of patients with secondary oxalate nephropathy.MethodsElectronic databases were searched for case reports and case series of individual cases or cohorts of patients with biopsy-proven oxalate nephropathy in native or transplanted kidneys from 1950 until January 2018.ResultsFifty-seven case reports and 10 case series met the inclusion criteria, totaling 108 patients. The case series were meta-analyzed. Mean age was 56.4 years old, 59% were men, and 15% were kidney transplant recipients. Fat malabsorption (88%) was the most commonly attributed cause of oxalate nephropathy, followed by excessive dietary oxalate consumption (20%). The mean baseline serum creatinine was 1.3 mg/dl and peaked at 4.6 mg/dl. Proteinuria, hematuria, and urinary crystals was reported in 69%, 32%, and 26% of patients, respectively. Mean 24-hour urinary oxalate excretion was 85.4 mg/d. In addition to universal oxalate crystal deposition in tubules and/or interstitium, kidney biopsy findings included acute tubular injury (71%), tubular damage and atrophy (69%), and interstitial mononuclear cell infiltration (72%); 55% of patients required dialysis. None had complete recovery, 42% had partial recovery, and 58% remained dialysis-dependent. Thirty-three percent of patients died.ConclusionSecondary oxalate nephropathy is a rare but potentially devastating condition. Renal replacement therapy is required in >50% of patients, and most patients remain dialysis-dependent. Studies are needed for effective preventive and treatment strategies in high-risk patients with hyperoxaluria-enabling conditions.

Lost in Transportation: Calcium Oxalate Crystals in Kidney Biopsy Specimens Fixed in Michel Medium May Disappear

“…While patient outcomes in acute or chronic renal injury with scattered CaOx crystals are variable and depend on the underlying condition, 2,4 the prognosis of oxalate nephropathy is generally poor, with more than half of patients progressing to end-stage kidney disease. 5,6 Additionally, if the diagnosis is missed and the underlying cause of hyperoxalosis is not corrected, the disease may also recur in the renal allograft following transplant as previously reported. 2,3 Our study is based on biopsies in which MTM was used to preserve kidney tissue for IF.…”

Review on Mineral Malabsorption and Reducing Technologies

“…Oxalate is an anti-nutrient which under normal conditions is confined to separate compartments. However, when it is processed and/or digested, it comes into contact with the nutrients in the gastrointestinal tract when released, oxalic acid binds with nutrients, rendering them inaccessible to the body [40].…”

Metabolism oxalic acid: failure causes and consequences of molecular-biochemical factors for the formation of oxalate-induced diseases

“…Вторинні порушення обміну ЩК виникають в силу екзогенних (надлишкове надходження оксалогенних продуктів, низький питний режим, збільшення споживання натрію та білка тварин, дефіцит магнію, вітамінів В2 і В6, ентеральна гіперабсорбція, наявність захворювань шлунковокишкового тракту) і ендогенних причин (спадкова схильність, порушення обміну амінокислот, нестабільність цитомембран або посилена ендогенна продукція, що виникає внаслідок впливу її попередників) [48,49,50].…”