scholarly journals Case Report: Hemolysis in a G6PD-deficient patient, a dose-dependent effect of metformin

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 1234
Author(s):  
Yusra Irshad ◽  
Mahum Nadeem ◽  
Usman Khan ◽  
Ezza Tariq ◽  
Aemen Khakwani
Keyword(s):  
Genetic Disorder ◽  
Middle Eastern ◽  
Kidney Injury ◽  
Cumulative Effect ◽  
Hemodynamic Instability ◽  
Phosphate Deficiency ◽  
White Blood Count ◽  
Dose Dependent ◽  
Dose Dependent Effect

Glucose-6-phosphate deficiency is an X-linked genetic disorder, which predisposes erythrocytes to oxidative stress, resulting in hemolysis. It is the most common enzymatic deficiency, and typically affects African, Asian, Mediterranean, and Middle Eastern lineages. It can be induced by some medications, chemicals, and foods. Metformin is an uncommon drug to cause hemolysis in G6PD-deficient patients. We report a case of a 52-year old African American male with G6PD-related hemolysis secondary to toxic metformin accumulation with acute kidney injury (AKI). The patient was a type-2 diabetic and was taking metformin (500mg twice daily) for three years. He presented to the ER with nausea, vomiting, and diarrhea for last three days with severe hemodynamic instability. Labs revealed hemoglobin 15mg/dl, white blood count 28 mm3/L, creatinine 10 mg/dl, blood urea nitrogen 100 mg/dl, bicarbonate 7 mEq/L, lactic acid 17 mg/dl, pH 6.8, pCO2 21mmHg, metformin 41 mcg/ml, albumin-globulin 41. Severe sepsis protocol was activated; IV fluids 30ml/kg bolus and antibiotics were given. CT abdomen revealed colitis. The patient was started on continuous renal replacement therapy. The next day, the patient’s hemoglobin dropped to 12.6 mg/dl. A hemolytic panel was unswerving with hemolysis and G6PD levels reported low at 1.72. The patient improved with antibiotics, but the hemolysis continued. Metformin toxicity induced hemolysis was suspected. The patient’s hemoglobin dropped to 6g/dl and he received blood transfusions. His hemoglobin started to improve with hemodialysis sessions, as metformin levels started to normalize, emphasizing the fact that patient was clearing metformin. Unlike most cases reported, in which hemolysis occurs within days to months of starting metformin, in our patient it occurred due to the cumulative effect of metformin because of the patient’s underlying AKI. This led us to propose that the hemolytic effect of metformin may not only be time-dependent but also dose-dependent.

Dose-Dependent Effect of Statins on the Incidence of Acute Kidney Injury After Cardiac Surgery

2011 ◽  
Vol 91 (2) ◽  
pp. 520-525 ◽  
Author(s):  
Salima Mithani ◽  
Michael Kuskowski ◽  
Yelena Slinin ◽  
Areef Ishani ◽  
Edward McFalls ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Kidney Injury ◽  
Dependent Effect ◽  
Dose Dependent ◽  
Dose Dependent Effect

scholarly journals Mutation in the SLC2A9 Gene: A New Family with Familial Renal Hypouricemia Type 2

2021 ◽  
Vol 2021 ◽  
pp. 1-3
Author(s):  
Christian Maalouli ◽  
Karin Dahan ◽  
Arnaud Devresse ◽  
Valentine Gillion
Keyword(s):  
Acute Kidney Injury ◽  
Genetic Disorder ◽  
Kidney Injury ◽  
Type Ii ◽  
Renal Hypouricemia ◽  
New Family ◽  
Exercise Induced ◽  
Renal Tubular ◽  
Work Up

Familial renal hypouricemia is a rare genetic disorder characterized by a defect in renal tubular urate reabsorption. Some patients present with exercise-induced acute kidney injury and nephrolithiasis. Type II is caused by mutations in the SLC2A9 gene. Here, we report the case of a young patient who developed acute kidney injury after exercise secondary to familial renal hypouricemia type II. The same mutation was found in other asymptomatic members of his family. We review the medical literature on this condition. This case highlights the importance of considering uric acid disorders in the work-up of acute kidney injury after exercise.

scholarly journals Exendin-4 disrupts responding to reward predictive incentive cues in rats

2018 ◽  
Author(s):  
Ken T. Wakabayashi ◽  
Ajay N. Baindur ◽  
Malte Feja ◽  
Karie Chen ◽  
Kimberly Bernosky-Smith ◽  
...  
Keyword(s):  
Weight Loss ◽  
Receptor Agonist ◽  
Drug Effect ◽  
Sucrose Reward ◽  
Reward Seeking ◽  
Seeking Behavior ◽  
Mesolimbic Dopamine Pathway ◽  
Dose Dependent ◽  
Dose Dependent Effect

AbstractExendin-4 (EX4) is a GLP-1 receptor agonist used clinically to control glycemia in Type-2 Diabetes Mellitus (T2DM), with the additional effect of promoting weight loss. The weight loss seen with EX4 is attributable to the varied peripheral and central effects of GLP-1, with contributions from the mesolimbic dopamine pathway that are implicated in cue-induced reward seeking. GLP-1 receptor agonists reduce preference for palatable foods (i.e. sweet and fat) as well as the motivation to obtain and consume these foods. Accumulating evidence suggest that GLP-1 receptor activity can attenuate cue-induced reward seeking behaviors. In the present study, we tested the effects of EX4 (0.6, 1.2, and 2.4 µg/kg i.p.) on incentive cue (IC) responding. This rat model required rats to emit a nosepoke response during an intermittent audiovisual cue to obtain a sucrose reward (10% solution). EX4 dose-dependently attenuated responding to reward predictive cues, and increased latencies of the cue response and reward cup entry to consume the sucrose reward. Moreover, EX4 dose-dependently decreased the number of nosepokes relative to the number of cue presentations during the session. There was no drug effect on the number of reward cup entries per reward earned during the session, a related reward-seeking behavior with similar locomotor demand. Interestingly, there was a dose-dependent effect of time on the responding to reward predictive cues and nosepoke response latency, such that 2.4 µg/kg of EX4 delayed responding to the initial IC of the behavioral session. Together, these findings suggest that agonism of the GLP-1 receptor with EX4 modulates the incentive properties of cues attributed with motivational significance.

Evaluating the Proposed Mechanism by Which Atorvastatin Can Protect Renal Tissue against Contrast Media: An Animal study

2019 ◽  
pp. 75-84
Keyword(s):  
Contrast Media ◽  
Kidney Injury ◽  
Saline Group ◽  
Pleiotropic Effect ◽  
Renal Tissue ◽  
Male Rats ◽  
Dependent Manner ◽  
Group 2 ◽  
Dose Dependent ◽  
Media Group

Contrast- induced nephropathy (CIN) is an elevation of serum creatinine of ≥ 0.5 mg/dL from baseline after two to three days of exposure to contrast substance if there is no other cause for acute kidney injury. Atorvastatin may protect normal kidney physiology from contrast- induced kidney injury by effects unrelated to hypolipidemia termed pleiotropic effect by decline of endothelin production, angiotensin system down regulation, and under expression of endothelial adhesion molecules. This study was conducted to assess the strategy by which atorvastatin can achieve protective effect for kidneys after exposure to contrast media in an animal model. A 40 male rats were distributed randomly into 4 groups; ten rats for each: group (1): given normal saline; group (2): CIN group given iopromide as contrast media; group (3): given atorvastatin (20mg/kg) and iopromide; and group (4): given atorvastatin (40mg/kg) and iopromide. Blood collected by cardiac puncture for detection of serum glutathione, malondialdehyde, matrix metalloproteinase-9, and interleukin-18. The results have shown a significant increase in inflammatory and oxidative stress markers in contrast media group, and significant reduction in these markers in atorvastatin treated groups, in a dose-dependent manner. As conclusion, atorvastatin mechanism for protection against CIN in a dose-dependent manner can mediate by anti-inflammatory and antioxidant effects.

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