ascorbic-acid and Nephritis--Interstitial

Acute kidney injury (AKI) is common among hospitalized patients with Coronavirus Infectious Disease 2019 (COVID-19), with the occurrence of AKI ranging from 0.5% to 80%. The variability in the occurrence of AKI has been attributed to the difference in geographic locations, race/ethnicity, and severity of illness. AKI among hospitalized patients is associated with increased length of stay and in-hospital deaths. Even patients with AKI who survive to hospital discharge are at risk of developing chronic kidney disease or end-stage kidney disease. An improved knowledge of the pathophysiology of AKI in COVID-19 is crucial to mitigate and manage AKI and to improve the survival of patients who developed AKI during COVID-19. The goal of this article is to provide our current understanding of the etiology and the pathophysiology of AKI in the setting of COVID-19.

Topics: Acute Kidney Injury; Anti-Bacterial Agents; Antiviral Agents; Apolipoprotein L1; Ascorbic Acid; Azotemia; COVID-19; COVID-19 Drug Treatment; Cytokines; Disease Progression; Glomerulonephritis; Glomerulonephritis, Membranous; Hospital Mortality; Humans; Kidney Tubules, Proximal; Length of Stay; Myoglobin; Nephritis, Interstitial; Nephrosis, Lipoid; Renal Insufficiency, Chronic; Rhabdomyolysis; SARS-CoV-2; Severity of Illness Index; Thrombotic Microangiopathies; Vitamins

A 48-year-old Japanese woman previously in good health was found to have severe proximal tubular dysfunction with a high serum level of ascorbic acid (57.3 microg/ml, reference range: 1.9 - 15.0 microg/ml). Renal biopsy specimen showed marked tubulointerstitial damage, i.e. tubular atrophy, dilatation of tubular lumen with flattened tubular epithelial cells, vacuolization of proximal and distal tubular epithelial cells, and severe interstitial fibrosis with mild infiltration of mononuclear cells. Calcified lesions, which caused tubular obstruction or stenosis, were also seen in interstitial area adjacent to degenerated proximal tubuli. Hypokalemic nephropathy, probably due to long-term use of laxatives, was clearly shown. However, calcified lesions seemed to be caused by inappropriate excessive daily ingestion of ascorbic acid (6 000 mg/day), calcium lactate, and vitamin D because of the patient's misunderstanding that these supplements could keep her in a good health. This condition may be clinically called "supplement nephropathy".

Topics: Ascorbic Acid; Biopsy; Calcium Compounds; Cathartics; Dietary Supplements; Dose-Response Relationship, Drug; Female; Follow-Up Studies; Humans; Kidney Glomerulus; Lactates; Middle Aged; Nephritis, Interstitial; Time Factors; Vitamin D; Vitamins

Topics: Aged; Ascorbic Acid; Biopsy; Female; Humans; Kidney Glomerulus; Nephritis, Interstitial; Uremia

Secondary oxalosis in chronic hemodialyzed patients is caused by impaired renal excretion and inadequate removal of oxalic acid during hemodialysis. Ascorbic acid is a precursor of oxalic acid. We report a parathyroidectomized patient with chronic renal failure, on hemodialysis, who received over a period of several months a total dose of 91.0 g ascorbic acid i.v. The plasma oxalic acid level in this patient was 14-fold higher than in healthy persons. Increased oxalic acid synthesis from its precursor ascorbic acid may be responsible for hyperoxalemia, high content of oxalic acid in myocardium, aorta and lung, and calcium oxalate deposition in soft tissues. Application of high doses of ascorbic acid should be avoided in hemodialysed patients with chronic renal failure.

Topics: Adult; Aorta; Ascorbic Acid; Calcinosis; Calcium Oxalate; Cardiomyopathies; Humans; Hyperparathyroidism, Secondary; Lung; Male; Nephritis, Interstitial; Parathyroid Glands; Renal Dialysis; Uremia