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Abstract: A 84-year-old women underwent renal biopsy because of rapidly progressive renal failure. Rabeprazole induced interstitial nephritis was diagnosed. Interstitial nephritis may complicate the course of any proton pump inhibitor treatment. It is a rare and serious complication. Clinician''s awareness of this adverse event is essential for early diagnosis and prompt recovery. [Copyright &y& Elsevier]

We used electronic medical record (EMR) data in the National Patient-Centered Clinical Research Network (PCORnet) to characterize "real-world" prescription patterns of Type 2 diabetes (T2D) medications. We identified a retrospective cohort of 613,203 adult patients with T2D from 33 datamarts (median patient number: 12,711) from 2012 through 2017 using a validated computable phenotype. We characterized outpatient T2D prescriptions for each patient in the 90 days before and after cohort entry, as well as demographics, comorbidities, non-T2D prescriptions, and clinical and laboratory variables in the 730 days prior to cohort entry. Approximately half of the individuals in the cohort were females and 20% Black. Hypertension (60.3%) and hyperlipidemia (50.5%) were highly prevalent. Most patients were prescribed either a single T2D drug class (42.2%) or had no evidence of a T2D prescription in the EMR (42.4%). A smaller percentage was prescribed multiple T2D drug types (15.4%). Among patients prescribed a single T2D drug type, metformin was the most common (42.6%), followed by insulin (18.2%) and sulfonylureas (13.9%). Newer classes represented approximately 13% of single T2D drug type prescriptions (dipeptidyl peptidase-4 inhibitors [6.6%], glucagon-like peptide-1 receptor agonists [2.5%], thiazolidinediones [2.0%], and sodium-glucose cotransporter-2 inhibitors [1.6%]). Among patients prescribed multiple T2D drug types, the most common combination was metformin and sulfonylureas (63.5%). Metformin-based regimens were highly prevalent in PCORnet's T2D population, whereas newer agents were prescribed less frequently. PCORnet is a novel source for the potential conduct of observational studies among patients with T2D., (© 2020 The Authors. Pharmacology Research & Perspectives published by John Wiley & Sons Ltd, British Pharmacological Society and American Society for Pharmacology and Experimental Therapeutics.)

Aluminum intoxication in chronic hemodialysis patients has virtually vanished over the last decade. Therefore, the diagnosis is rarely advocated at present. Aluminum intoxication in dialysis patients associates to different degrees with dialysis encephalopathy, bone disorders and microcytic anemia. We report here the observation of a patient receiving intermittent hemodialysis therapy who presented with acute encephalopathy. It turned out to be caused by aluminum intoxication secondary to a defect in dialysis water treatment. Whatever the therapeutic approach, the prognosis of this dramatic complication in hemodialysis patients remains poor. In severe cases, only renal transplantation can be able to improve clinical outcome. Major sources of aluminum are tap water used for dialysis together with a defective water treatment system, and to a minor extent oral aluminum-containing phosphate binders and antacids. In the absence of a bone biopsy, the diagnosis can be made by measuring serum aluminum or better after a desferrioxamine test. Prevention of aluminum overload is of utmost importance. It is the responsibility of dialysis centers to provide aluminum-free water and dialysis fluid. In case of proven aluminum intoxication, the K/DOQI guidelines indicated how to best treat hemodialysis patients, based on long-term desferrioxamine infusions during the hemodialysis session. It is recommended to implement a stepwise increasing desferrioxamine dosage to prevent an acute decompensation with irreversible neurological lesions., (Copyright © 2017 Société francophone de néphrologie, dialyse et transplantation. Published by Elsevier Masson SAS. All rights reserved.)

A 84-year-old women underwent renal biopsy because of rapidly progressive renal failure. Rabeprazole induced interstitial nephritis was diagnosed. Interstitial nephritis may complicate the course of any proton pump inhibitor treatment. It is a rare and serious complication. Clinician's awareness of this adverse event is essential for early diagnosis and prompt recovery.

The effects of thrombin perfusion on glomerular fibrinolytic activity (GFA) have been assessed quantitatively in isolated rat glomeruli. Gfa was augmented by increasing total thrombin perfused to a maximal dose of 120 units per 100 gm. Fifty per cent maximal GFA occurred at a dose of 38 to 42 units of thrombin per 100 gm. independent of duration or rate of perfusion. After termination of infusion, GFA diminished and thrombi were no longer observed. Simultaneous administration of thrombin and epsilon-aminocaproic acid was associated with sustained high GFA and persistence of thrombi, presumably due to inhibition of the action of plasmin on fibrin, but it had no effect on tissue activators of plasminogen.

The hypocalciuric effect of phosphorus or hydrochlorothiazide therapy was evaluated in 26 hypercalciuric stone-formers after 2 to 4 months and 8 to 12 months treatment. After 2 to 4 months, a significant decrease of the urinary calcium to creatinine ratio was noted only in a group of 7 patients receiving phosphorus supplementation (1500 mg/day). The decrease was transient however, since in 5 of these patients, the calcium to creatinine ratio was found to be at pretreatment levels when the patients were reinvestigated after 8 to 12 months on phosphorus. In contrast, in 8 patients receiving hydrochlorothiazide (50 mg/day) during 8 to 12 months, this ratio was significantly lower (P less than 0.01) than before treatment. A group of patients maintained on high water intake alone for 8 to 12 months served as a control and no modification in calcium excretion was observed. This study indicates that long-term treatment with hydrochlorothiazide is more efficient in lowering urinary calcium excretion than phosphorus therapy.

During aetiological investigation of recently developed hypertension in a 31-year-old man, isolated dissection of the upper branch of the right renal artery was discovered. Injection, after sodium depletion, of saralasin, a competitive angiotensin II inhibitor, resulted in significant fall of the mean arterial pressure. During sodium depletion, the plasma renin activity was higher in the right renal artery (17.8 ng/ml/h) than in the left artery (9.4 ng/ml/h) and the infra-renal portion of the inferior vena cava (8.7 ng/ml/h). These figures suggested that surgical treatment of the dissection would have beneficial effects on blood pressure. Six months after resection of the pathological arterial segment and replacement by a graft from the internal saphenous vein, blood pressure had spontaneously returned to normal levels.

Eleven patients with kidney stone disease and idiopathic hypercalciuria (urinary calcium above 4 mg/kg/j), without phosphorus renal leak and 6 control subjects have been put for 3 days on a diet containing 1 g calcium and 1 phosphorus daily (period A), and then for 4 days on a diet containing 1 g calcium, 450 mg phosphorus and 3 g aluminium hydroxyde daily (period B). During period A, no significant difference in blood calcium, phosphorus and magnesium, not in phosphaturia, rate of phosphorus reabsorption (RPR) and ratio maximum RPR/creatinine clearance was found between the two groups. After 2 days on a low phosphate diet (period B) the blood phosphorus decreased significantly in the hypercalciuric patients but not in the control subjects, thus revealing among the forme a latent abnormality in the retention of phosphates. This abnormality could play an important role in the pathogenesis of hypercalciuria.

We report on 4 cases of reversible acute renal failure (ARF), appearing within the first days after institution of a sulfinpyrazone treatment (600 mg p. day) early after a myocardial infarction. Urinary data were consistent with an acute tubular necrosis. A renal biopsy, performed in 3 patients, revealed only very discrete tubular and interstitial lesions, not helpful in the understanding of the ARF. Three pathogenetic mechanisms could be evoked. Data in favour of an acute tubular precipitation of uric acid or an immunologically induced acute interstitial nephritis are lacking. More probably this ARF is due to an inhibitory effect of sulfinpyrazone on the renal prostaglandin synthesis. Early after a myocardial infarction, renal prostaglandins could play an important protective role in maintaining the renal circulation. Renal function should be monitored closely when sulfinpyrazone is prescribed, especially early after a myocardial infarction.