losartan-potassium and Hyperoxaluria

Ascorbate supplementation for patients on regular dialysis treatment (RDT) is advised to obviate deficiency and improve epoetin response in those with functional iron deficiency. However, clear-cut safety concerns regarding hyperoxalemia are still poorly understood. This study tries to establish safety/efficacy profiles of ascorbate and oxalate during long-term intravenous ascorbate supplementation.. A prospective study was performed in 30 patients on RDT showing ascorbate deficiency (plasma ascorbate < 2.6 mg/L [<15 micromol/L]): 18 patients were administered intravenous ascorbate during 18 months (250 mg/wk, subsequently increased to 500 mg), and 12 patients were taken as reference untreated cases. Plasma ascorbate and oxalate assays and dialytic balance determinations were performed (ion chromatography and reverse-phase high-performance liquid chromatography, respectively) at baseline, during treatment, and 12 months after withdrawal.. Plasma ascorbate levels increased dose dependently with supplementation (1.6 +/- 0.8 mg/L [9.1 +/- 4.6 mumol/L] at baseline, 2.8 +/- 1.8 mg/L [15.9 +/- 10.1 micromol/L]) with 250 mg of ascorbate, and 6.6 +/- 2.8 mg/L [37.5 +/- 16.0 micromol/L] with 500 mg/wk of ascorbate), but only normalized with greater dosages for several months in 94% of patients. Baseline plasma oxalate levels increased from 3.2 +/- 0.8 mg/L (35.8 +/- 8.8 micromol/L) to 3.6 +/- 0.8 mg/L (39.5 +/- 9.1 micromol/L) and 4.5 +/- 0.9 mg/L (50.3 +/- 10.4 micromol/L) with 250 and 500 mg, respectively ( P < 0.001). The calcium oxalate saturation threshold was exceeded by 7 of 18 patients (40%) during 6 months therapy with 500 mg/wk. Ascorbate dialysis removal increased from 37.8 +/- 23.2 mg (215 +/- 132 micromol) to 99.6 +/- 51.7 mg (566 +/- 294 micromol) during supplementation (P < 0.001), with corresponding increases in oxalate removal from 82.5 +/- 33.2 mg (917 +/- 369 micromol) to 111.2 +/- 32.6 mg/L (1,236 +/- 362 micromol; P < 0.01). Withdrawal reverted plasma levels and dialysis removal to initial values. Values for untreated patients did not change during 1 year of follow-up.. Patients on RDT may resolve ascorbate deficiency with intravenous supplementation of 500 mg/wk, but this implies a significant risk for oxalate supersaturation. Oxalate measurements are strongly recommended during long-term ascorbate therapy.

Topics: Adult; Aged; Aged, 80 and over; Anemia; Ascorbic Acid; Ascorbic Acid Deficiency; Calcium Oxalate; Drug Resistance; Erythropoietin; Female; Humans; Hyperoxaluria; Infusions, Intravenous; Kidney Failure, Chronic; Male; Middle Aged; Prospective Studies; Renal Dialysis

Primary hyperoxaluria is a rare autosomal recessive disorder. Type 1 PH is the most common form and develops due to a defect in a liver specific enzyme the alanine aminotransferase enzyme. As a result of the enzyme deficiency, there is an overproduction of oxalate and excessive urinary excretion. Recurrent urolithiasis and nephrocalcinosis are the most important findings of the disorder and often at the beginning end-stage renal disease develops. This report presents a case backed up by literature of a patient with end stage renal failure and erythropoietin-resistant anaemia whose bone marrow biopsy showed crystal deposition which received delayed diagnosis of oxalosis.

Topics: Adult; Anemia; Bone Marrow; Erythropoietin; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Kidney Failure, Chronic; Male

Anemia is an important cause of morbidity in patients suffering from chronic renal failure, and erythropoietin is a milestone of anemia treatment. Various factors may cause erythropoietin resistance. Herein, we describe the case of 32-year-old man who presented with anemia and weakness. He developed progressive renal failure secondary to recurrent kidney stones. One year before admission, he developed anemia for which he had been treated with erythropoietin. However, the anemia persisted. Examination of bone marrow biopsy specimen showed that the marrow was extensively replaced with oxalate crystals and fibrous connective tissue with severe decrease of hematopoietic cells. To the best of our knowledge, our patient represents the first case in the literature describing the association between the oxalate deposition and EPO resistance.

Topics: Adult; Anemia; Biopsy, Needle; Bone Marrow Diseases; Chronic Disease; Drug Resistance; Erythropoietin; Follow-Up Studies; Humans; Hyperoxaluria; Immunohistochemistry; Kidney Calculi; Kidney Failure, Chronic; Male; Oxalates; Renal Dialysis; Risk Assessment; Severity of Illness Index; Treatment Failure