Alfredo Peguero

Vitamin C-induced oxalate nephropathy.

Although a multitude of syndromes have been thoroughly described as a result of vitamin deficiencies, over consumption of such substances may also be quite dangerous. Intratubular crystallization of calcium oxalate as a result of hyperoxaluria can cause acute renal failure. This type of renal failure is known as oxalate nephropathy. Hyperoxaluria occurs as a result of inherited enzymatic deficiencies known as primary hyperoxaluria or from exogenous sources known as secondary hyperoxaluria. Extensive literature has reported and explained the mechanism of increased absorption of oxalate in malabsorptive syndromes leading to renal injury. However, other causes of secondary hyperoxaluria may also take place either via direct dietary consumption of oxalate rich products or via other substances which may metabolize into oxalate within the body. Vitamin C is metabolized to oxalate. Oral or parenteral administration of this vitamin has been used in multiple settings such as an alternative treatment of malignancy or as an immune booster. This article presents a clinical case in which ingestion of high amounts of vitamin C lead to oxalate nephropathy. This article further reviews other previously published cases in order to illustrate and highlight the potential renal harm this vitamin poses if consumed in excessive amounts.

Baclofen Toxicity in Patients with Advanced Nephropathy: Proposal for New Labeling

Background: Despite several reports in the literature of baclofen toxicity in patients with renal dysfunction, the drug is being used for many patients. Methods: Herein we report a case of baclofen-induced encephalopathy in a patient with pre-end-stage renal disease and review the literature regarding the magnitude of baclofen toxicity in patients with renal insufficiency. A Medline search for studies in English was performed. Twenty-one case reports involving 41 patients (including our patient) were identified. Results: The majority of patients were elderly (62.5% above 60 years) males (56.3%) on dialysis (62.9%). Neurotoxicities were almost always present at presentation. Manifestations of baclofen toxicity usually started 2–3 days after starting baclofen; however, periods as long as 16 weeks have been reported. The daily dose of baclofen ranged from 5 to 60 mg with a mean dose of 20 mg. Hemodialysis (HD) was the most common treatment modality used for drug elimination (65.7%). The recovery time ranged from 2 h in patients who received HD, to 8 days with conservative treatment. Conclusion: The literature does not mention a clear recommendation about baclofen safety and dose adjustment, or a minimum level of kidney function below which the drug should not be used.

A case of selective immunoglobulin M deficiency and autoimmune glomerulonephritis

Immunodeficiency states have been implicated in autoimmune diseases. Early recognition of these states is important because prophylaxis can prevent morbidity and mortality. The following is a case report of a 57-year-old male who presented with recurrent infections. He was found to have IgM deficiency. All of his infections were treated appropriately with successful responses. He developed glomerulonephritis, which was read by the pathologist as post-infectious glomerulonephritis. Despite antibiotic therapy, his renal function never recovered, leading to permanent hemodialysis. The patient’s renal biopsy exhibited histological features compatible with a membrano-proliferative glomerulonephritis. Retrospectively, it is likely that this patient had autoimmune glomerulonephritis, explaining his failure to respond to antimicrobials.

Serum cystatin C versus serum creatinine in the estimation of glomerular filtration rate in rhabdomyolysis.

Cystatin C has emerged as a possible, usable surrogate marker of renal function. We present a case that illustrates the clinical utility of cystatin C in the setting of acute kidney injury secondary to rhabdomyolysis. An African American male whose baseline cystatin C and serum creatinine levels taken a month prior to admission were compared against their daily values during his admission and at follow up. On admission, the patients reduction in glomerular filtration rate (GFR) from baseline was much less when calculated with cystatin C than with serum creatinine. His clinical recovery was more reflective of the higher GFR with cystatin C than what would be assumed with his serum creatinine, which at its worst was 5 ml/min/1.73 m(2). The patient was eventually discharged from the hospital with a GFR of 40 ml/min by cystatin C despite his GFR by the MDRD equation being 12. Cystatin C may be a more accurate marker of the both the amount of injury and the rate of resolution of acute kidney injury than serum creatinine in rhabdomyolysis.

Anti-MPO small-vessel vasculitis causing prostatis and nephritis.

Microscopic polyangiitis is a necrotizing angiitis involving capillaries, venules, and arterioles. The vascular beds of various organs may be involved, causing varying presentations. To our knowledge, this is the first case of anti-myeloperoxidase (anti-MPO) antibody small-vessel vasculitis causing prostatic vasculitis. A 79 year-old nonsmoker American man presented with symptoms of fevers, malaise, weight loss, and cough. Urine analysis revealed hematuria. Blood tests were remarkable for an elevated prostate-specific antigen (PSA) and a serum creatinine of 3.1 mg/dl (baseline, 1.2 mg/dl). Computed tomography (CT) scan of the thorax revealed a 4.7-cm mass in the left lower lobe of the lung. Metastatic prostate cancer was suspected. Therefore, prostatic biopsy was performed. The biopsy revealed fibrinoid degeneration with vasculitic changes involving the arterioles. When evaluated by nephrology, his serum creatinine was 9.9 mg/dl. A renal biopsy was performed, which revealed focal segmental necrotizing glomerulopathy with microscopic vasculitis. All the serologies were normal, with the exception of low C4, and positive perinuclear antineutrophil cytoplasmic antibodies (ANCA) associated with anti-MPO. The patient was started on intermittent hemodialysis, steroids, and oral cytoxan. Despite treatment, with improvement of the respiratory and constitutional symptoms, the patient remained dialysis-dependent. He later decided to discontinue dialysis and subsequently expired. Vasculitic involvement of the prostate is an uncommon manifestation of microscopic polyangiitis. This bedazzling entity is challenging to diagnose and thus makes it difficult to treat in a timely manner.

D-Glucose and NaCl Enhance the Expression of Aquaporin-1: Inhibition of Both by Cholera Toxin

Aim: To determine whether glucose, NaCl and/or cholera toxin modify the expression of aquaporin-1 (AQP-1) water channel. Methods: Aquaporin-1 gene expression was studied using primary cultures of human renal proximal tubule epithelial (HRPTE) cells. Results:D-Glucose and NaCl (500 mosm/kg·H2O each) enhanced AQP-1 expression 2.4-fold (p < 0.05) and 4.0-fold (p < 0.01), respectively, which could be blocked 73 and 70% (p < 0.01), respectively, by cholera enterotoxin (10–7M). Angiotensin II (10–6M and 10–8M), vasopressin (10–8M) and/or atrial natriuretic peptide (10–8M) did not affect AQP-1 expression. Hyperosmolar Reno-60 and Hypaque-76 contrast agents at 500 mosm/kg·H2O and isomolar Visipaque at 25% (v/v) concentration(s) also increased AQP-1 expression 3.8- to 5.0-fold (p < 0.01) in HRPTE cells which also were inhibited by cholera toxin from 41% (p < 0.05) to 71% (p < 0.01). AQP-1 was translocated from the cytosol to the membrane of HRPTE cells and hyperosmolarity enhanced this translocation 2.5-fold (p < 0.01). Conclusions: The increased urinary concentrating ability in proximal segment of the diabetic kidney associated with increased plasma glucose may be mediated via glucose’s ability to enhance AQP-1 expression, which leads to a more concentrated urine. The decrease in urinary flow secondary to cholera toxin exposure, on the other hand, may be mediated indirectly by cholera toxin’s inhibition of aquaoporin-1 gene expression.