diabetestalk.net

Renal Tubular Acidosis Metformin

Metformin Protects Renal Tubular Cells; Mechanisms And Newconcepts

Metformin Protects Renal Tubular Cells; Mechanisms And Newconcepts

Metformin protects renal tubular cells; mechanisms and newconcepts 1 Department of Surgery, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran 2 Social Determinants of Health Research Center, Yasuj University of Medical Sciences, Yasuj, Iran 3 Medical Student Research Committee and Social Determinant of Health Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran 4 Department of Pediatrics, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran 5 Cancer Prevention Research Center, Isfahan University of Medical Sciences, Isfahan, Iran 6 Department of Radiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran *Corresponding author: Mohammad Davoodi; Email: Email: [email protected] Context: The prevalence of diabetes markedly increased in recent decades. It is well acceptedthat the risk of morbidity and fatality increases in patients with type 2 diabetes (T2DM). Evidence Acquisition: An electronic search was performed to detect suitable studies, withkeywords of metformin, prediabetes, diabetes Mellitus, Gentamicin and lactic acidosis. Results: Metformin (biguanide) is widely used as the first pharmacological option inpre-diabetic subjects and patients with T2DM. Low-cost, long-term effect, low risk ofhypoglycemia, and ease in utilization are considered as significant benefits of metformincompared with other therapies. Numerous studies have explored that medicinalintervention particularly metformin administration not only can decrease high bloodglucose in patients with T2DM but also can avoid or postpone the beginning of clinicalT2DM in pre-diabetic cases. Protective effect of metformin on renal cells by differentmechanisms is described here. Gentamici Continue reading >>

Spotlight: A Case Of Metformin Associated Lactic Acidosis

Spotlight: A Case Of Metformin Associated Lactic Acidosis

1. What is metformin-associated lactic acidosis? 2. How does severe acidemia lead to acute kidney injury? 3. How do you treat metformin-associated lactic acidosis? The patient is a 40-year-old man with alcohol dependence and type II diabetes who presented to the emergency department for alcohol intoxication. After arriving hemodynamically stable with reassuring labs, he become tachypneic, confused, and lethargic a few hours later. At this point, he admitted that he took a few metformin pills in a suicide attempt. Arterial blood gas was significant for a pH < 6.8 and a lactate > 22 mg/dL. Due to this decompensation, he was intubated, admitted to the medical ICU, and started on hemodialysis via a newly-placed hemodialysis catheter. He was later transitioned to continuous veno-venous hemofiltration, after which his lactic acidosis resolved. Upon stopping hemodialysis, however, the patients creatinine continued to steadily rise, so he was transferred to general medicine for further management. On arrival to general medicine, an initial urinalysis showed hematuria with red blood cells and granular casts but no red blood cell casts. Given the unclear diagnosis, a renal biopsy was done demonstrating acute tubular necrosis overlying mesangial IgA deposition, consistent with acute kidney injury in the setting of newly diagnosed IgA nephropathy. Acute tubular necrosis was thought to be the result of acidemia-induced hypotension. The patients creatinine levels continued to downtrend steadily and he was discharged home with plans for renal and psychiatric follow-up. 1. What is metformin-associated lactic acidosis? Metformin, an antihyperglycemic biguanide, is a commonly used diabetic medication that increases glucose utilization by promoting insulin binding to insulin receptors in Continue reading >>

[lactic Acidosis And Severe Hyperkalemia In A Diabetic Patient Treated With Metformin And Enalapril: Influence Of Acute Renal Disease And Drugs].

[lactic Acidosis And Severe Hyperkalemia In A Diabetic Patient Treated With Metformin And Enalapril: Influence Of Acute Renal Disease And Drugs].

[Lactic acidosis and severe hyperkalemia in a diabetic patient treated with metformin and enalapril: influence of acute renal disease and drugs]. Unit Operativa di Diabetologia e Malattie Metaboliche, PMAO-Ospedale di Circolo e Fondazione Macchi, Varese. A 71 year old hypertensive and non insulin-dependent diabetic patients with moderate renal insufficiency taking 500 mg/d of metformin and 5 mg/d of enalapril, developed metabolic acidosis characterized by fairly elevated anion gap, hyperchloremia, severe hyperkalemia, normal plasma level of beta-hydroxybutyric acid, absence of ketonuria and high plasma level of lactic acid. This biochemical feature allowed us to ascribe the pathogenesis of metabolic acidosis both to the increased plasma level of lactic acid and to the type IV renal tubular acidosis syndrome, the precipitating factor being an infection of urinary tract (as we assumed on the basis of the urine culture). The patient was dehydrated and lethargic; the ECG revealed the presence of nonparoxysmal junctional tachycardia. The clinical evolution was favorable thanks to the treatment with the infusion of isotonic saline solutions, mild alkalinizing solutions, low-dose regular insulin and antibiotics. It is likely that metformin and enalapril, regularly assumed by the patient, could have played a iatrogenic role even if they were taken in low dosages. This event points out the importance of complying with the indications and especially the contraindications of these drugs, to avoid life threatening complications as that one occurred in this case. Continue reading >>

Metformin-associated Lactic Acidosis: A Case Report

Metformin-associated Lactic Acidosis: A Case Report

Metformin-Associated Lactic Acidosis: A Case Report A 54-year-old woman with type 2 diabetes mellitus, hypertension, and peripheral vascular disease developed life-threatening lactic acidosis during treatment with metformin for type 2 diabetes. The woman received metformin at 1000mg orally twice a day for type 2 diabetes. She presented to our emergency department with a 3-day history of severe watery diarrhea, nausea, and vomiting. Her grandson whom she cared for had gastroenteritis several days prior to the onset of her symptoms. She was confused and hypotensive with a blood pressure of 70/39mmHg. Her initial laboratory findings were remarkable with an arterial blood gas pH 6.57, HCO\( _{3}^{ - } \) 2mEq/L, anion gap 30mmol/L, and lactate 16.3mmol/L. She was diagnosed with severe lactic acidosis. Metformin was discontinued. Upon arrival in the emergency department, she became unresponsive and experienced a pulseless electrical activity cardiac arrest. After resuscitation, her severe acidemia persisted despite aggressive intervention with volume resuscitation and vasopressors, leading to the initiation of renal replacement therapy. After multiple dialysis treatments, her severe acidemia resolved. Serum metformin concentration from presentation ultimately returned to 42 mcg/mL (therapeutic concentration: 12 mcg/mL). She was discharged from the hospital on day 15 without any neurologic complications. A Naranjo assessment score of 8 was obtained, indicating a probable relationship between the patients lactic acidosis and her use of the suspect drug. Metformin toxicity should be considered in any patient with type 2 diabetes mellitus presenting with severe lactic acidosis and profound acidemia. Metformin-associated lactic acidosis can be treated with renal replacement ther Continue reading >>

Case Study: Metformin-associated Lactic Acidosis

Case Study: Metformin-associated Lactic Acidosis

Could orlistat be relevant? Lactic acidosis is a rare (1) but serious complication of metformin therapy with a high fatality rate (2). In the majority of reported cases there is a preexisting disease, most often a degree of renal impairment. We present a case of metformin-associated lactic acidosis (MALA) where drug interactions (orlistat in the long term and cimetidine over a short period of time) may have potentiated the condition. A 59-year-old woman with type 2 diabetes for 14 years presented with a history of 3 months of vague abdominal pain and four to five loose bowel movements daily, which worsened over the 4 days before admission to hospital. On the day of admission she reported weakness, dizziness, and blurred vision. Her husband had noticed slurred speech and a reduced level of consciousness. There was a past history of a healed duodenal ulcer and obesity. She had documented normal renal function 4 months before this admission (urea 5.7 mmol/l and creatinine 105 μmol/l). Her diabetes was well controlled on metformin at 500 mg t.i.d. for the past 8 years. Three months before admission she started orlistat at 120 mg t.i.d., which coincided with the onset of the abdominal pain and chronic diarrhea. During the 4 days before admission, as her abdominal pain worsened, cimetidine (400 mg b.i.d.) was prescribed on the presumption of reactivation of her duodenal ulcer. Clinical examination showed an obese woman who was agitated and confused, with a Glasgow Coma Scale of 10/15. She was apyrexial, with a pulse of 70 bpm in sinus rhythm, blood pressure 85/40 mmHg, and O2 saturation 97% on air. General examination was otherwise unremarkable; in particular there was no evidence of diabetic retinopathy or neuropathy. Preliminary laboratory investigations showed a life-thre Continue reading >>

Metformin-associated Lactic Acidosis In An Intensive Care Unit

Metformin-associated Lactic Acidosis In An Intensive Care Unit

Metformin-associated lactic acidosis in an intensive care unit Peters et al.; licensee BioMed Central Ltd.2008 Metformin-associated lactic acidosis (MALA) is a classic side effect of metformin and is known to be a severe disease with a high mortality rate. The treatment of MALA with dialysis is controversial and is the subject of many case reports in the literature. We aimed to assess the prevalence of MALA in a 16-bed, university-affiliated, intensive care unit (ICU), and the effect of dialysis on patient outcome. Over a five-year period, we retrospectively identified all patients who were either admitted to the ICU with metformin as a usual medication, or who attempted suicide by metformin ingestion. Within this population, we selected patients presenting with lactic acidosis, thus defining MALA, and described their clinical and biological features. MALA accounted for 0.84% of all admissions during the study period (30 MALA admissions over five years) and was associated with a 30% mortality rate. The only factors associated with a fatal outcome were the reason for admission in the ICU and the initial prothrombin time. Although patients who went on to haemodialysis had higher illness severity scores, as compared with those who were not dialysed, the mortality rates were similar between the two groups (31.3% versus 28.6%). MALA can be encountered in the ICU several times a year and still remains a life-threatening condition. Treatment is restricted mostly to supportive measures, although haemodialysis may possess a protective effect. Since the UK Prospective Diabetes Study was published in 1998, metformin has become the standard of care for overweigh patients with diabetes [ 1 ]. Indeed, metformin has been shown to reduce the rate of cardiovascular disease within this Continue reading >>

Can Metformin Cause Renal Tubular Acidosis?

Can Metformin Cause Renal Tubular Acidosis?

Lamisil vs Lotrimin Mucinex vs Sudafed Lactogen 1 Side Effects Evekeo vs Adderall Dexilant and Alcohol Treato does not review third-party posts for accuracy of any kind, including for medical diagnosis or treatments, or events in general. Treato does not provide medical advice, diagnosis or treatment. Usage of the website does not substitute professional medical advice. The side effects featured here are based on those most frequently appearing in user posts on the Internet. The manufacturer's product labeling should always be consulted for a list of side effects most frequently appearing in patients during clinical studies. Talk to your doctor about which medications may be most appropriate for you. The information reflected here is dependent upon the correct functioning of our algorithm. From time-to-time, our system might experience bugs or glitches that affect the accuracy or correct application of mathematical algorithms. We will do our best to update the site if we are made aware of any malfunctioning or misapplication of these algorithms. We cannot guarantee results and occasional interruptions in updating may occur. Please continue to check the site for updated information. Continue reading >>

Diabetes Mellitus And Hyperkalemic Renal Tubular Acidosis: Case Reports And Literature Review

Diabetes Mellitus And Hyperkalemic Renal Tubular Acidosis: Case Reports And Literature Review

Diabetes mellitus and hyperkalemic renal tubular acidosis: case reports and literature review Carlos Henrique Pires Ratto TavaresBello 1 Hyporeninemic hypoaldosteronism, despite being common, remains an underdiagnosed entity that is more prevalent in patients with diabetes mellitus. It presents with asymptomatic hyperkalemia along with hyperchloraemic metabolic acidosis without significant renal function impairment. The underlying pathophysiological mechanism is not fully understood, but it is postulated that either aldosterone deficiency (hyporeninemic hypoaldosteronism) and/or target organ aldosterone resistance (pseudohypoaldosteronism) may be responsible. Diagnosis is based on laboratory parameters. Treatment strategy varies according to the underlying pathophysiological mechanism and etiology and aims to normalize serum potassium. Two clnical cases are reported and the relevant literature is revisited. Keywords:acidosis; acidosis, renal tubular; diabetes mellitus; hyperkalemia; hypoaldosteronism Renal tubular acidosis (RTA) comprises relatively frequent forms of hyperchloremic metabolic acidosis. This medical condition is underdiagnosed and poorly understood due to the complexity of the involved pathophysiological mechanisms. It is characterized by the occurrence of hyperchloremic metabolic acidosis, fluid and electrolyte balance disorders (involving potassium in particular), and absence of significant renal impairment. The glomerular filtration rate (GFR) of affected individuals is relatively preserved, while tubular impairment is the main element responsible for the observed alterations. Renal tubular acidosis is divided into three forms of involvement: Type 1 RTA (distal RTA) - impaired distal hydrogen ion secretion. Type 2 RTA (proximal RTA) - impaired proxima Continue reading >>

Renal Tubular Acidosis (rta)

Renal Tubular Acidosis (rta)

By L. Aimee Hechanova, MD, Assistant Professor of Medicine, Texas Tech University; Attending Nephrologist, University Medical Center (See also Introduction to Disorders of Kidney Tubules .) In renal tubular acidosis, the kidney tubules malfunction, resulting in excess levels of acid in the blood. The tubules of the kidneys that remove acid from the blood are damaged when a person takes certain drugs or has another disorder that affects the kidneys. Often muscle weakness and diminished reflexes occur when the disorder has been present for a long time. Blood tests show high acid levels and a disturbance of the body's acid-base balance. Some people drink a solution of baking soda every day to neutralize the acid. To function normally, body acids and alkali (such as bicarbonate) must be balanced. Normally, the breakdown of food produces acids that circulate in the blood. The kidneys remove acids from the blood and excrete them in the urine. This function is predominantly carried out by the kidney tubules . In renal tubular acidosis, the kidney tubules malfunction in one of two ways that tend to increase acids in the blood ( metabolic acidosis ): Too little of the acids the body produces are excreted, so acid levels in blood increase. Too little of the bicarbonate that filters through the kidney tubules is reabsorbed, so too much bicarbonate is lost in the urine. In renal tubular acidosis, the balance of electrolytes is also affected. Renal tubular acidosis may lead to the following problems: Low or high potassium levels in the blood Calcium deposits in the kidneys, which may lead to kidney stones Painful softening and bending of the bones (osteomalacia or rickets ) Renal tubular acidosis may be a permanent, inherited disorder in children. However, it may be an intermittent Continue reading >>

Management Of Metformin-associated Lactic Acidosis By Continuous Renal Replacement Therapy

Management Of Metformin-associated Lactic Acidosis By Continuous Renal Replacement Therapy

Management of Metformin-Associated Lactic Acidosis by Continuous Renal Replacement Therapy Affiliations Hospices Civils de Lyon, Groupement Hospitalier Edouard Herriot, Service de Ranimation Mdicale, Lyon, France, Universit de Lyon, Universit Lyon 1, Facult de mdecine Lyon-Est, Lyon, France Affiliations Hospices Civils de Lyon, Groupement Hospitalier Edouard Herriot, Service de Ranimation Mdicale, Lyon, France, Universit de Lyon, Universit Lyon 1, Facult de mdecine Lyon-Est, Lyon, France Affiliation Hospices Civils de Lyon, Groupement Hospitalier Edouard Herriot, Service de Ranimation Mdicale, Lyon, France Affiliation Hospices Civils de Lyon, Groupement Hospitalier Edouard Herriot, Service de Ranimation Mdicale, Lyon, France Affiliations Hospices Civils de Lyon, Groupement Hospitalier Edouard Herriot, Service de Ranimation Mdicale, Lyon, France, Universit de Lyon, Universit Lyon 1, Facult de mdecine Lyon-Est, Lyon, France Affiliations Hospices Civils de Lyon, Groupement Hospitalier Edouard Herriot, Service de Ranimation Mdicale, Lyon, France, Universit de Lyon, Universit Lyon 1, Facult de mdecine Lyon-Est, Lyon, France Continue reading >>

Xigduo Xr (dapagliflozin,metformin) Dosage, Indication, Interactions, Side Effects | Empr - Renal And Urology News

Xigduo Xr (dapagliflozin,metformin) Dosage, Indication, Interactions, Side Effects | Empr - Renal And Urology News

Moderate-to-severe renal impairment (eGFR <60mL/min/1.73m2), ESRD, or on dialysis. Metabolic acidosis, diabetic ketoacidosis. Increased risk of metformin-associated lactic acidosis in renal or hepatic impairment, concomitant use of certain drugs (eg, cationic drugs), 65yrs of age, undergoing radiological contrast study, surgery and other procedures, hypoxic states, and excessive alcohol intake; discontinue if lactic acidosis occurs. Discontinue at time of, or prior to intravascular iodinated contrast imaging in patients with a history of hepatic impairment, alcoholism, heart failure, or will be given intra-arterial contrast; reevaluate eGFR 48hrs after procedure and restart therapy if renally stable. Correct volume depletion before initiating. Monitor for symptomatic hypotension in renal impairment (eGFR <60mL/min/1.73m2), elderly, low systolic BP, or on loop diuretics. Assess for ketoacidosis in presence of signs/symptoms of metabolic acidosis, regardless of blood glucose levels; discontinue if suspected, evaluate and treat; consider risk factors before initiation (eg, pancreatic insulin deficiency, caloric restriction, alcohol abuse). Assess renal function prior to starting and periodically thereafter; more frequently in elderly. Risk of acute kidney injury in hypovolemia, chronic renal insufficiency, CHF, and concomitant drugs (eg, diuretics, ACEIs, ARBs, NSAIDs). Consider temporarily discontinuing in reduced oral intake or fluid losses; monitor for acute kidney injury; discontinue and treat if occurs. Elderly, debilitated, uncompensated strenuous exercise, malnourished or deficient caloric intake, adrenal or pituitary insufficiency, or alcohol intoxication: increased risk of hypoglycemia. Monitor for genital mycotic infections, UTIs, hematology (esp. serum Vit. B12 Continue reading >>

Metabolic Effects Of Metformin In Patients With Acute Renal Failure

Metabolic Effects Of Metformin In Patients With Acute Renal Failure

Metformin use has been associated with significant disturbances in acid-base balance. Metformin remains the first-line therapy for majority of patients with type 2 diabetes mellitus. Its metabolic effects have provided great support for its use in diabetes management. However, risks of renal impairment and lactic acidosis have always warranted close monitoring in patients with predisposing factors to these events. In fact, lactic acidosis has been associated with renal impairment. Metformin is not metabolized in the liver and is excreted by active tubular secretion. The risk of developing lactic acidosis greatly depends on the magnitude of each patient’s renal impairment and their age. Nonetheless, these studies fail to take into consideration those patients with renal failure. The majority of trials out there exclude patients with renal defects due to its nephrotoxic potential. The nephrotoxicity of increased levels of metformin relies on its effect on renal mitochondrial activity. Previous studies have demonstrated that therapeutic doses of metformin are not associated with risk of lactic acidosis. Renal mitochondrial dysfunction can lead to tubular cell ischemia and increased lactic acid production. Hence, those patients with renal impairment will warrant closer monitoring and dose optimization strategies to prevent these complications while obtaining optimal glucose control. Recently, renal dose adjustments changed. Now patients are to be monitored based on glomerular filtration rate and not serum creatinine for metformin therapy. A recent study conducted by David Cucchiari and colleagues evaluated the dose-related effects of metformin on acid-base balance in patients with diabetes who develop acute renal failure. In this cross-sectional study, 126 patients were i Continue reading >>

Drug-induced Metabolic Acidosis

Drug-induced Metabolic Acidosis

Go to: Introduction Metabolic acidosis is defined as an excessive accumulation of non-volatile acid manifested as a primary reduction in serum bicarbonate concentration in the body associated with low plasma pH. Certain conditions may exist with other acid-base disorders such as metabolic alkalosis and respiratory acidosis/alkalosis 1. Humans possess homeostatic mechanisms that maintain acid-base balance ( Figure 1). One utilizes both bicarbonate and non-bicarbonate buffers in both the intracellular and the extracellular milieu in the immediate defense against volatile (mainly CO 2) and non-volatile (organic and inorganic) acids before excretion by the lungs and kidneys, respectively. Renal excretion of non-volatile acid is the definitive solution after temporary buffering. This is an intricate and highly efficient homeostatic system. Derangements in over-production, under-excretion, or both can potentially lead to accumulation of excess acid resulting in metabolic acidosis ( Figure 1). Drug-induced metabolic acidosis is often mild, but in rare cases it can be severe or even fatal. Not only should physicians be keenly aware of this potential iatrogenic complication but they should also be fully engaged in understanding the pathophysiological mechanisms. Metabolic acidosis resulting from drugs and/or ingestion of toxic chemicals can be grouped into four general categories ( Figure 2): Some medications cannot be placed into one single category, as they possess multiple mechanisms that can cause metabolic acidosis. In suspected drug-induced metabolic acidosis, clinicians should establish the biochemical diagnosis of metabolic acidosis along with the evaluation of respiratory compensation and whether there is presence of mixed acid-based disorders 2, then convert the bioche Continue reading >>

Renal Tubular Acidosis Due To Oxaliplatin

Renal Tubular Acidosis Due To Oxaliplatin

Oxaliplatin is a third-generation platinum derivative which in combination with a fluoropyrimidine has demonstrated improved overall survival in metastatic colon cancer [ 1 ], prolonged progression free survival in an adjuvant setting [ 2 ] and prompted recommendations for its use by the National Institute for Clinical Excellence [ 3 ]. Initial studies with oxaliplatin did not identify significant renal toxicity but acute tubular necrosis (without dehydration) has been reported [ 4 ]. This is a case of a 53-year-old gentleman who developed severe renal tubular acidosis, probably secondary to oxaliplatin. Duke's B adenocarcinoma of the transverse colon (pT4N0, stage II) was diagnosed following hemicolectomy for perforated bowel in 2002. After 6 months of adjuvant therapy with 5-flourouracil (425 mg/m2 on days 15, repeated every 28 days for 6 cycles), he re-presented in 2005 with weight loss and a solitary liver metastasis was identified by TELSA MRI and FDG PET-CT. He was commenced on neo-adjuvant oxaliplatin (130 mg/m2 on day 1 q21d) and capecitabine (1000 mg/m2 BD on days 114, q21d) before hepatic resection. On day 14 of the second cycle of oxaliplatin and capecitabine, he was admitted with a 7-day history of lethargy, anorexia, nausea, polyuria and increasing breathlessness. His oral intake had been 23 litres of salt lassi (pH 4) and three or four limes a day. He had a past medical history of type 2 diabetes treated with metformin and hypercholesterolaemia treated with simvastatin. On examination, he was dehydrated, flushed, and tachypnoiec although the chest was clear. An arterial blood gas revealed a severe metabolic acidosis with partial respiratory compensation ( Table 1 , day 1). Serum K+ and Cl were 3.3 mmol/l and 113 mmol/l, respectively. Moderate ketones were Continue reading >>

Metformin Challenges In Advanced Chronic Kidney Disease: A Promising Therapeutic Strategy

Metformin Challenges In Advanced Chronic Kidney Disease: A Promising Therapeutic Strategy

Metformin Challenges in Advanced Chronic Kidney Disease: A Promising Therapeutic Strategy M. Fidalgo Daz * , R. Alonso Valente, V. Becerra Mosquera, I. Abuward, S. Puello Martnez, N. Ardha, M. Durn Beloso, D. Novoa Garca, T. Cordal Martnez, D. Gimil Carbajal, C. Daz Rodrguez Department of Nephrology, Hospital Clnico Universitario de Santiago de Compostela, Spain Received Date: July 12, 2017; Accepted Date: August 16, 2017; Published Date: August 18, 2017 Citation: Daz MF, Valente RA, Mosquera VB, Abuward I, Martnez SP, et al. (2017) Metformin Metformin Challenges in Advanced Chronic Kidney Disease. A Promising Therapeutic Strategy. Jour Ren Med. Vol.1 No.2: 12. Visit for more related articles at Journal of Renal Medicine Background: Metformin is the first-line treatment in type 2 diabetes mellitus because the beneficial effects respect to other antidiabetic drugs on hypoglycemia, obesity, dyslipidemia and cardiovascular morbidity and mortality and even on renal cancer incidence. However, the accumulation of metformin in cases of impaired renal function may lead to a type B lactic acidosis, which has led to its contraindication in patients with chronic kidney disease (CKD), initially to glomerular filtration less than 60 ml/min and subsequently less than 30 ml/min. The dosedependent toxicity, the low rate of onset of metforminassociated lactic acidosis (MALA) and lack of knowledge of pharmacokinetics in CKD, have motivated the development of studies which could support metformin use in advanced stages of CKD. Methods: We did a literature review compiling recent, more relevant and impact articles, to conclude about the current situation of metformin safety in advanced stages of CKD as well as try to offer a concise future perspective. The analysis has been structured abo Continue reading >>

More in diabetes