Diet-induced oxalate nephropathy

Oxalate Nephropathy Caused by Excessive Vitamin C Administration in 2 Patients With COVID-19

Enteric hyperoxaluria, nephrolithiasis, and oxalate nephropathy: potentially serious and unappreciated complications of Roux-en- Y gastric bypass

SAT-460 HISTOLOGICAL DIAGNOSIS OF HYPEROXALURIA FROM RENAL BIOPSY

Introduction: Oxalate nephropathy (ON) is a rare condition involving the precipitation of calcium oxalate crystals within the nephrons. Primary hyperoxaluria involves enzymatic defects in the metabolism of glyoxylate, while secondary hyperoxaluria includes dietary and malabsorption-related etiologies. Case presentation: We discuss the case of a White male in his 80s who presented to the hospital with acute kidney injury on chronic kidney disease stage 4 in the setting of a new antibiotic prescription. Creatinine had increased to 4.2 mg/dL from a baseline of 2.2 mg/dL, with no etiology identified on urinalysis or renal ultrasound. Renal biopsy then revealed an acute tubular injury with intraluminal calcium oxalate crystals deposits, confirming a diagnosis of ON. Discussion: A detailed history revealed an excessive dietary intake of oxalate-rich foods, including nuts, and daily ingestion of 2 g of vitamin C. The patient was counselled on adjusting his diet and stopping vitamin C supplementation, which led his creatinine to return close to baseline 2 months post-discharge. Conclusion: Thorough history-taking enables early recognition and timely interventions to possibly avoid hyperoxaluria from progressing to end-stage kidney disease (ESRD).

Oxalate nephropathy: a three-dimensional view

NALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy

Oxalate nephropathy is a relatively rare and under-recognized condition that commonly presents as acute kidney injury (AKI) and often leads to end-stage renal disease. Complete recovery of kidney function is extremely rare even when treatment is instituted early on. We present the case of a 68-year-old man with known type 2 diabetes mellitus and an asymptomatic unrecognized exocrine pancreatic insufficiency, who was admitted due to dialysis-dependent AKI. Kidney biopsy revealed oxalate nephropathy. A wide diagnostic assessment and a multi-factorial treatment plan that included a change of diet, therapy for exocrine pancreatic insufficiency and fat malabsorption, sodium bicarbonate and potassium citrate, calcium supplements with meals, and methylprednisolone, resulted in complete recovery of kidney function. It is important for physicians to be aware of oxalate nephropathy in cases of prolonged AKI. After confirmation of diagnosis, a wide diagnostic approach is imperative to identify all the causes that have led to oxalosis. A multi-factorial therapeutic approach can lead to complete kidney recovery.

BackgroundCalcium oxalate nephropathy is rare in current practice. It was a common complication during jejunoileal bypass, but much less seen in modern gastric bypass surgery for morbid obesity. The major cause of it is enteric hyperoxaluria.Case presentationWe report on a patient here with acute kidney disease due to calcium oxalate nephropathy, rather than the conditions mentioned above. The male patient received a Roux-en Y hepaticojejunostomy and common bile duct drainage. In addition to enteric hyperoxaluria, chronic kidney disease related metabolic acidosis, chronic diarrhea related volume depletion, a high oxalate and low potassium diet, long term ascorbic acid intake and long term exposure to antibiotics, all predisposed him to having oxalate nephropathy.ConclusionThis is the first case with such conditions and we recommend that similarly diagnosed patients avoid all these predisposing factors, in order to avoid this rare disease and its undesired outcome.

Intravenous albumin is recommended for hepatorenal disorders (HRD), but individuals who do not recover renal function may be at a high risk for pulmonary edema. We reviewed outcomes by the amount of albumin infused in 93 patients not receiving dialysis at admission but being treated with intravenous albumin for acute HRD at our institution. Absence of renal recovery was defined as no decrease in serum creatinine and requirement of dialysis during hospitalization, and partial renal recovery was defined as a decrease in serum creatinine but not to prehospitalization levels. Associations of clinical factors including total albumin infused, presence of renal recovery, and oliguria with the development of pulmonary edema during hospitalization were determined using logistic regression. Of the 93 patients, 20 patients had complete renal recovery, 17 patients had partial renal recovery, and 56 patients showed no renal recovery. Most patients received 300–600 g of albumin. Overall, 47.3% of patients developed pulmonary edema (n=44), but the risk was 75% in patients with oliguria on presentation and no renal recovery versus 17% in those with no oliguria and complete renal recovery (P<0.001). In the logistic regression model, oliguria (3.32; 95% confidence interval [CI]: 1.12, 9.81) and no renal recovery (3.38; 95% CI:1.24, 9.16) were each associated with higher odds of pulmonary edema after adjustment for covariates. No association was noted between total albumin infused and pulmonary edema. In summary, absence of renal recovery and oliguria in patients with HRD receiving intravenous albumin is associated with a higher risk of pulmonary edema.

Hyperoxaluria Is a Long-Term Consequence of Roux-en-Y Gastric Bypass: A 2-Year Prospective Longitudinal Study

Intrarenal crystals trigger inflammation and renal cell necroptosis, processes that involve TNF receptor (TNFR) signaling. Here, we tested the hypothesis that TNFRs also have a direct role in tubular crystal deposition and progression of hyperoxaluria-related CKD. Immunohistochemical analysis revealed upregulated tubular expression of TNFR1 and TNFR2 in human and murine kidneys with calcium oxalate (CaOx) nephrocalcinosis-related CKD compared with controls. Western blot and mRNA expression analyses in mice yielded consistent data. When fed an oxalate-rich diet, wild-type mice developed progressive CKD, whereas Tnfr1-, Tnfr2-, and Tnfr1/2-deficient mice did not. Despite identical levels of hyperoxaluria, Tnfr1-, Tnfr2-, and Tnfr1/2-deficient mice also lacked the intrarenal CaOx deposition and tubular damage observed in wild-type mice. Inhibition of TNFR signaling prevented the induced expression of the crystal adhesion molecules, CD44 and annexin II, in tubular epithelial cells in vitro and in vivo, and treatment with the small molecule TNFR inhibitor R-7050 partially protected hyperoxaluric mice from nephrocalcinosis and CKD. We conclude that TNFR signaling is essential for CaOx crystal adhesion to the luminal membrane of renal tubules as a fundamental initiating mechanism of oxalate nephropathy. Furthermore, therapeutic blockade of TNFR might delay progressive forms of nephrocalcinosis in oxalate nephropathy, such as primary hyperoxaluria.

Background and Aims Cystinuria is considered a rare condition as approximately 1% of adult and 6% of pediatric kidney stones are due to this defect. Prevalence varies by geographic region, with good representation in the Mediterranean area. Given the low prevalence and the lack of a defined clinical pathway for these patients, only partial data are available on the long-term course of the disease. A group of cystinuria patients has gathered on Facebook to exchange advice on symptom management and therapy. The use of this type of platform, in cases of low-prevalence diseases, is a good method of collecting patients who otherwise would be difficult to reach. We proposed an online survey to further analyze clinical, therapy, and quality of life of cystinuria patients. Method An online survey was proposed to an Italian social media group restricted to cystinuric patients with the agreement of the administrator. Before participating to the survey, patients provided documentation on their diagnosis and signed an informed consent. The survey was structured in four sections: a thorough medical history focused on kidney stone and cystinuria, the SF-36 questionnaire, the Fatigue Severity Scale, The Brief Pain Inventory. Data was managed and analyzed anonymously. Results Our survey was sent to 55 patients, but only 18 completed all questionnaires. Our cohort is composed of 5 men and 13 women, with a mean age of 39.5 years (SD 17.6), mean height 156.4 cm (SD 18.5), mean weight 60.8 kg (SD 17.9), mean BMI 24.1 (SD 4.5). About medical history, 15/18 patients have had at least 4 episodes of renal sstons in their lifetime, of these 10/15 reported stone expulsion in most episodes. The first episode occurred on average at 14.9 years (SD 9.3), while confirmed diagnosis of cystinuria arises at 20.1 years (SD 15.1). Most patients experienced bilateral stones (12/18). The diagnosis was confirmed generally by: stone composition analysis (39%), urinary cystine levels (24%), cystine crystals revealed at fresh urine exam (22%), genetic findings (7%), Brand test (2%), other (5%). About 33% of our cohort performed a genetic test. Almost 95% of patients are in follow-up with a clinic. Routine exams include: renal ultrasound (30%), nephrologist evaluation (27%), urine 24h evaluation (25%), urology visit (13%), abdominal CT (4%), kidney x-ray (2%). All the patients of our cohort received urological or surgical procedures for kidney stones: generally endoscopic procedures (32%), or lithotripsy (30%), or open surgery (23%). Four patients underwent a nephrectomy. Patienst reportes an average of 31 painful episodes of renal colic (min 0; max 200) in their history. Of these episodes almost 6 ended with a stone expulsion (min 0; max 50), while haematuria was reported by 12 patients (up to 20 episodes in a patient lifetime). A secondary stone composition in addition to cystine was reported by 5/18: calcium oxalate in 100% of these cases, even with struvite and calcium phosphate. Most of these patients (78%) received some nutritional recommendation: generally by nephrologist (50%), or dietician (23%), or urologist (18%). Indications were not easy to follow: a 0-100 visual scale about compliance showed a mean of 45 (SD 27). The 78% were currently on drug therapy: most used therapy included citrate (45%), tiopronin (40%), or bicarbonate (10%). Drugs compliance is very low (26/100 scale SD 23.3). Nobody in our cohort showed a GFR of less than 60 mL/min/1.73 m2. 4/18 reported a positive family history of cystinuria, while 7/18 relatives with renal stones without a diagnosis. Conclusion Patients affected by cystinuria show a very poor quality of life, with high levels of pain, fatigue, and emotional wellness. The diagnosis is delayed from the first event, and they are exhausted by an high frequency of pain stone passages. More attention to quality of life aspects is needed in patients with this rare but life-threatening condition.

Background Acute kidney injury (AKI) is considered as a common and significant complication following abdominal aortic aneurysm (AAA) repair. This study aimed to assess the associated risk factors of AKI in the critically ill patients undergoing AAA repair and to evaluate the appropriate AKI management in the specific population. Methods We retrospectively examined data from all critically ill patients undergoing AAA repairs at our institution from April 2007 to March 2012. Multivariable analysis was used to identify factors associated with postoperative AKI, which was defined by risk, injury, failure, loss and end-stage (RIFLE) kidney disease criteria. The goal-directed hemodynamic optimization (maintenance of optimal hemodynamics and neutral or negative fluid balance) and renal outcomes were also reviewed. Results Of the 71 patients enrolled, 32 (45.1%) developed AKI, with 30 (93.8%) cases diagnosed on admission to surgical intensive care unit (SICU). Risk factors for AKI were ruptured AAA (odds ratio (OR)=5.846, 95% confidence interval (CI): 1.346-25.390), intraoperative hypotension (OR=6.008, 95% CI: 1.176 to 30.683), and perioperative blood transfusion (OR=4.611, 95% CI: 1.307-16.276). Goal-directed hemodynamic optimization resulted in 75.0% complete and 18.8% partial renal recovery. Overall in-hospital mortality was 2.8%. AKI was associated with significantly increased length of stay ((136.9±24.5) hours vs. (70.4±11.3) hours) in Surgical Intensive Care Unit. Conclusions Critically ill patients undergoing AAA repair have a high incidence of AKI, which can be early recognized by RIFLE criteria. Rupture, hypotension, and blood transfusion are the significant associated risk factors. Application of goal-directed hemodynamic optimization in this cohort appeared to be effective in improving renal outcome.

Introduction: There is no information in literature specifically on the prevalence and clinicopathological characteristics of acute tubulointerstitial nephritis/drug induced acute kidney injury (AKI) from Pakistan.Objectives: We aim to report a series of cases from patients developing AKI after exposure to some medications or finding of interstitial nephritis on histopathology.Patients and Methods: This is an observational study of patients identified as having AKI after exposure to medications. AKI was defined according to RIFLE criteria and all patients fell from risk to loss category on arrival. On ultrasonography, all patients had normal size non-obstructed kidneys. Renal biopsy findings were consistent with tubule interstitial nephritis.Results: Mean age of patients was 36.41 ± 17.40 years. Among total of 155, 80 were male and 75 female. Regarding drugs, most common was exposure to aminoglycoside in 34 (22%) followed by use of non-steroidal anti-inflammatory analgesics in 28, contrast induced agents in 11. Renal biopsy was performed in 58 patients. In half of these, insulting agent was not known and in rest either multiple medications were ingested or there was denial to substance use or recovery was delayed despite discontinuation of responsible medication. Renal replacement therapy was required on arrival in 119/155 (hemodialysis = 115, peritoneal dialysis = 4) cases. Complete renal recovery was observed in 71%, while 7.7% expired during acute phase, partial renal recovery was seen in 15% and 5% disappeared after first discharge from the hospital.Conclusion: Tubulointerstitial nephritis may occur with many drugs of common use. Early and intensive efforts must be made to consider and then timely correct the injury to the kidney.

Pregnancy-related kidney injury contributes to a high burden of acute kidney injury in low-resource settings and causes maternal and perinatal morbidity and mortality. Few studies have examined the impact of acute kidney injury in resource-limited countries, with very limited research on pregnancy-specific disorders in Ethiopia. This study aimed to determine the characteristics of pregnancy-related acute kidney injury, outcomes and associated factors. A retrospective study was conducted to evaluate the clinical profile and maternal-fetal outcome of pregnancy-related acute kidney injury at Ayder Comprehensive Specialized Hospital in Tigray, Ethiopia, from January 1, 2017, to December 31, 2021. Maternal and fetal outcomes were analyzed using descriptive statistics. Multivariate logistic regression was used to determine the association between the dependent and independent variables. Of 27,350 mothers who delivered at Ayder Comprehensive Specialized Hospital between January 1, 2017, and December 31, 2021, a total of 187 women developed pregnancy-related acute kidney injury, a prevalence rate of 68 per 100,000 births. Preeclampsia, sepsis and pre-renal causes due to dehydration and hemorrhage were the most common causes of pregnancy-related acute kidney injury in this study. Hemodialysis was needed in 8.6% (n = 16) of patients. Of the 187 pregnancy-related acute kidney injuries, 143 (76.5%) recovered completely and 30 (16%) partially. The mortality rate was 7.5%. Preexisting chronic kidney disease (AOR = 30.13; 95% CI: 2.92, 310.84), use of vasoactive agents (AOR = 5.77; 95% CI: 1.47, 22.67), increase in creatinine per unit (AOR = 1.65; 95% CI: 1.11, 2.45) and complications related to acute kidney injury (AOR = 5.26; 95% CI: 1.73, 16.00) were determinants of the composite endpoints (partial renal recovery and death). This study emphasizes acute kidney injury in resource-limited settings is a significant cause of maternal and fetal morbidity and mortality. The vast majority of patients with pregnancy-related acute kidney injury recovered completely from kidney injury. The main causes of pregnancy-related acute kidney injury were preeclampsia, sepsis and pre-renal associated with hemorrhage and dehydration. Preexisting renal disease, use of vasopressors, increase in creatinine per unit and complications associated with acute kidney injury were determining factors for concomitant fetomaternal mortality. Appropriate preventive strategies during prenatal care and prompt treatment are needed for pregnancy-related acute kidney injury.