Abstract:Ethylene glycol (EG) is a sweet-tasting, odorless organic solvent found in many agents, such as anti-freeze. EG is composed of four organic acids: glycoaldehyde, glycolic acid, glyoxylic acid and oxalic acid in vivo. These metabolites are cellular toxins that can cause cardio-pulmonary failure, life-threatening metabolic acidosis, central nervous system depression, and kidney injury. Oxalic acid is the end product of EG, which can precipitate to crystals of calcium oxalate monohydrate in the tubular lumen and … Show more
“…Details of the case reports and case series that had short-term exposure to hyperoxularia-enabling conditions, and as result, were not included in the systematic review, are summarized in Supplementary Table S2 . 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 Figure 1 Study selection flow diagram. ASN, American Society of Nephrology.…”
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.
“…Details of the case reports and case series that had short-term exposure to hyperoxularia-enabling conditions, and as result, were not included in the systematic review, are summarized in Supplementary Table S2 . 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 Figure 1 Study selection flow diagram. ASN, American Society of Nephrology.…”
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.
“…These crystals may precipitate in the tubular lumen of the kidney causing an acute oxalate nephropathy. 6 Focal necrosis in the liver has also been reported. 7,8 Propylene glycol (propane-1,2-diol) is commonly used as a solvent in household domestic products and it is often used as a solvent in the pharmaceutical industry.…”
Section: Discussionmentioning
confidence: 97%
“…These crystals may precipitate in the tubular lumen of the kidney causing an acute oxalate nephropathy. 6 Focal necrosis in the liver has also been reported. 7,8…”
We report the case of an 18-year-old male admitted to the Intensive Care Unit in Basingstoke and North Hampshire Hospital, who developed chronic kidney disease following the ingestion of smoke machine fluid. Smoke machine fluid may contain ethylene glycol, and a diagnosis of ethylene glycol toxicity with calcium oxalate nephropathy was made. This case resulted in a National Poisons Information Service internal review of the subject and a new TOXBASE entry for smoke machine fluid ingestion.
KeywordsRenal failure, ethylene glycol, propylene glycol, smoke machine, haemofiltration
CaseWe report the case of an 18-year-old male presenting to the Emergency Department with vomiting and anuria following reported ingestion of 3 l of a fluid used in a smoke machine 35 h previously. The patient had mild learning difficulties and reported ingesting the liquid due to intrigue with no self-harm intent. He complained of nausea, vomiting and mild abdominal and back pain. He had been anuric for over 24 h.Blood results taken on admission showed a raised urea (6.1 mmol/l) and creatinine (176 mmol/l) with a normal full blood count and liver function tests on a background of a normal renal function. A venous blood gas showed a metabolic acidosis with a pH of 7.21, HCO À 3 15.3 mmol/l, BE 11.7 mmol/l, lactate 1.8 mmol/ l. An anion gap was calculated at 17.3 mEq/l (normal range: 3-11 mEq/l) and an osmolar gap was calculated at 4 mOsm/kg (normal range: <10 mOsm/kg). A diagnosis was made of acute kidney injury, possibly consistent with the metabolism of glycol products.The case was discussed with a toxicology consultant at the National Poisons Information Service (NPIS) who advised intravenous hydration and hemofiltration if renal function deteriorated. Fomepizole was not recommended by the NPIS and ethylene glycol levels were not measured.The metabolic acidosis continued to be static; however, the patient remained anuric and renal function continued to worsen.The patient was admitted to the intensive care unit (ICU) and Continuous Veno-Veno Haemofiltration with heparin anticoagulation was commenced. Liver function tests showed raised transaminases (ALT 278 u/l) and a raised amylase (685 u/l); coagulation tests remained normal. Following normalisation of transaminases citrate anticoagulation was commenced. He also developed hypertension (170/90 mmHg) requiring amlodipine and bisoprolol.A total of eight days of renal replacement therapy were required on ICU during which time he remained anuric before he was transferred to the regional renal unit. He remained on the regional renal unit for 20 days. His urine output recovered but further haemodialysis was required via a tunnelled RIJ central line. On day 14, he developed abdominal pain, which was traced to a 3-mm right mid-pole renal calculus, with a raised urinary oxalate. An episode of abdominal sepsis was treated with meropenem and vancomycin and resolved with no positive microbiology.
“…154 Necrosis of the renal proximal tubular cells can occur from internalized calcium oxalate monohydrate crystals in ethylene glycol toxicity and secondarily from hypotension, myoglobinuria, and hemoglobinuria in methanol toxicity. 155,156 A variety of drugs may result in movement disorders combined with renal dysfunction. For example, lithium toxicity manifests with action tremor, cerebellar ataxia, and renal involvement in the form of nephrogenic diabetes insipidus and reduction in glomerular filtration rate.…”
Movement disorders often emerge from the interplay of complex pathophysiological processes involving the kidneys and the nervous system. Tremor, myoclonus, ataxia, chorea, and parkinsonism can occur in the context of renal dysfunction (azotemia and electrolyte abnormalities) or they can be part of complications of its management (dialysis and renal transplantation). On the other hand, myoglobinuria from rhabdomyolysis in status dystonicus and certain drugs used in the management of movement disorders can cause nephrotoxicity. Distinct from these well-recognized associations, it is important to appreciate that there are several inherited and acquired disorders in which movement abnormalities do not occur as a consequence of renal dysfunction or vice versa but are manifestations of common pathophysiological processes affecting the nervous system and the kidneys. These disorders are the emphasis of this review. Increasing awareness of these conditions among neurologists may help them to identify renal involvement earlier, take timely intervention by anticipating complications and focus on therapies targeting common mechanisms in addition to symptomatic management of movement disorders. Recognition of renal impairment in a patient with complex neurological presentation may narrow down the differentials and aid in reaching a definite diagnosis.
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