Hyperuricemia ; Focus on Treatment
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Hyperuricemia, or elevated uric acid levels, can be caused by overproduction or under-excretion of uric acid. It is closely related to cardiovascular and renal complications and the development of gout. Treatment is recommended for patients with two or more acute gout attacks per year, the presence of tophi, chronic kidney disease stage 2 or higher, or kidney stones. The target uric acid level for treatment is less than 6 mg/dL. Management of hyperuricemia involves lifestyle changes like weight loss and dietary modifications as well as drug therapy with urate-lowering medications like allopurinol. Higher doses of allopurinol from 100-900 mg have been shown to improve endothelial function
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Hyperuricemia
This document discusses hyperuricemia, which is a high level of uric acid in the blood. It covers the following key points:
- Causes of hyperuricemia include overproduction of uric acid, underexcretion by the kidneys, or a combination of the two. Various medical conditions and medications can also cause hyperuricemia.
- Clinical presentations of hyperuricemia include gout (painful arthritis), uric acid kidney stones, and nephropathy. Gout typically starts as acute attacks of pain and swelling in joints like the big toe. Without treatment, gout can progress to chronic arthritis and tophi (hard lumps) under the skin.
Hyperuricemia and Gout
Hyperuricemia Lecture
Presented by Usama Ragab Youssif
For 5th-year medical students - Zagazig University
Hyperuricemia
Hyperuricemia is caused by high levels of uric acid in the blood and can be due to underexcretion of uric acid by the kidneys, overproduction of uric acid, or a combination of both. Underexcretion is the most common cause and can result from reduced kidney function or medications that impact excretion. Overproduction occurs when there is excessive breakdown of purines from foods or the body. Certain genetic disorders, tumors, or diets high in purines can lead to overproduction. Conditions like alcohol use, fructose intake, or rapid weight loss may cause both overproduction and underexcretion of uric acid.
Uric acid disorders
This document discusses normal and abnormal uric acid metabolism, conditions related to hyperuricemia such as gout and kidney disease, and treatments for hyperuricemia. It notes that uric acid is produced through purine breakdown and provides an overview of gout pathogenesis. It also summarizes the mechanisms, efficacy, dosing, and administration of the xanthine oxidase inhibitor drugs allopurinol and febuxostat which are used to lower uric acid levels and treat gout.
Hyperuricemia and gout
The document discusses hyperuricemia and gout. It defines hyperuricemia as a plasma urate concentration greater than 7.0 mg/dl and can result from increased urate production, decreased urate excretion, or a combination. Gout is caused by the deposition of monosodium urate crystals in the joints and other tissues, which can cause acute inflammatory arthritis. The first metatarsophalangeal joint is commonly affected. Treatment involves medications like colchicine, NSAIDs, or glucocorticoids for acute attacks and urate-lowering therapies for long-term management.
Gout and hyperuricemia
This document discusses hyperuricemia and gout. It defines hyperuricemia as an elevated level of uric acid in the blood. It then covers the etiology, epidemiology, diagnosis, risk factors, complications, prevention and treatment of both hyperuricemia and gout. Gout is described as a form of inflammatory arthritis that results from excess uric acid in the blood, causing sudden, severe pain and swelling in the joints. Common treatments include NSAIDs, colchicine, steroids, and allopurinol or febuxostat to reduce uric acid levels.
Pathophysiology and clinical management of gouty arthritis
Gout is the most common inflammatory joint disorder caused by deposition of urate crystals in joints. It affects around 1-2% of adults and is more common in men. Risk factors include genetics, diet high in purines, alcohol, obesity, and medications. Gout progresses through acute inflammatory attacks, intercritical periods, and chronic tophaceous stages if urate levels remain elevated. Treatment involves NSAIDs to rapidly alleviate acute attacks and urate-lowering drugs like allopurinol or febuxostat long-term to prevent future attacks and reduce urate levels. Lifestyle modifications and diet control are also important for gout management.
Iron Deficiency Anemia
Iron deficiency anemia (IDA) is common worldwide, affecting 2-20% of different populations in the US. IDA is caused by inadequate iron intake, impaired absorption, or physiologic losses. Screening for IDA is recommended for pregnant women and high-risk infants aged 6-12 months. A complete workup is needed when IDA is identified to determine the underlying cause. Serum ferritin level is the best initial diagnostic test, with levels below 25 ng/mL strongly indicating iron deficiency.
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Hyperuricemia
This document discusses hyperuricemia, which is a high level of uric acid in the blood. It covers the following key points:
- Causes of hyperuricemia include overproduction of uric acid, underexcretion by the kidneys, or a combination of the two. Various medical conditions and medications can also cause hyperuricemia.
- Clinical presentations of hyperuricemia include gout (painful arthritis), uric acid kidney stones, and nephropathy. Gout typically starts as acute attacks of pain and swelling in joints like the big toe. Without treatment, gout can progress to chronic arthritis and tophi (hard lumps) under the skin.
Hyperuricemia and Gout
Hyperuricemia Lecture
Presented by Usama Ragab Youssif
For 5th-year medical students - Zagazig University
Hyperuricemia
Hyperuricemia is caused by high levels of uric acid in the blood and can be due to underexcretion of uric acid by the kidneys, overproduction of uric acid, or a combination of both. Underexcretion is the most common cause and can result from reduced kidney function or medications that impact excretion. Overproduction occurs when there is excessive breakdown of purines from foods or the body. Certain genetic disorders, tumors, or diets high in purines can lead to overproduction. Conditions like alcohol use, fructose intake, or rapid weight loss may cause both overproduction and underexcretion of uric acid.
Uric acid disorders
This document discusses normal and abnormal uric acid metabolism, conditions related to hyperuricemia such as gout and kidney disease, and treatments for hyperuricemia. It notes that uric acid is produced through purine breakdown and provides an overview of gout pathogenesis. It also summarizes the mechanisms, efficacy, dosing, and administration of the xanthine oxidase inhibitor drugs allopurinol and febuxostat which are used to lower uric acid levels and treat gout.
Hyperuricemia and gout
The document discusses hyperuricemia and gout. It defines hyperuricemia as a plasma urate concentration greater than 7.0 mg/dl and can result from increased urate production, decreased urate excretion, or a combination. Gout is caused by the deposition of monosodium urate crystals in the joints and other tissues, which can cause acute inflammatory arthritis. The first metatarsophalangeal joint is commonly affected. Treatment involves medications like colchicine, NSAIDs, or glucocorticoids for acute attacks and urate-lowering therapies for long-term management.
Gout and hyperuricemia
This document discusses hyperuricemia and gout. It defines hyperuricemia as an elevated level of uric acid in the blood. It then covers the etiology, epidemiology, diagnosis, risk factors, complications, prevention and treatment of both hyperuricemia and gout. Gout is described as a form of inflammatory arthritis that results from excess uric acid in the blood, causing sudden, severe pain and swelling in the joints. Common treatments include NSAIDs, colchicine, steroids, and allopurinol or febuxostat to reduce uric acid levels.
Pathophysiology and clinical management of gouty arthritis
Gout is the most common inflammatory joint disorder caused by deposition of urate crystals in joints. It affects around 1-2% of adults and is more common in men. Risk factors include genetics, diet high in purines, alcohol, obesity, and medications. Gout progresses through acute inflammatory attacks, intercritical periods, and chronic tophaceous stages if urate levels remain elevated. Treatment involves NSAIDs to rapidly alleviate acute attacks and urate-lowering drugs like allopurinol or febuxostat long-term to prevent future attacks and reduce urate levels. Lifestyle modifications and diet control are also important for gout management.
Iron Deficiency Anemia
Iron deficiency anemia (IDA) is common worldwide, affecting 2-20% of different populations in the US. IDA is caused by inadequate iron intake, impaired absorption, or physiologic losses. Screening for IDA is recommended for pregnant women and high-risk infants aged 6-12 months. A complete workup is needed when IDA is identified to determine the underlying cause. Serum ferritin level is the best initial diagnostic test, with levels below 25 ng/mL strongly indicating iron deficiency.
Hyperuricemia in CKD
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Hyperuricemia and gout
The document discusses purine and pyrimidine metabolism and their role in genetic material replication, transcription, protein synthesis and cellular metabolism. It then focuses on hyperuricemia and gout, explaining that this results from increased uric acid production or impaired excretion. The key biochemical pathways of purine degradation to uric acid are described, as well as the factors influencing uric acid solubility and excretion by the kidneys through specific transporters. The causes, clinical manifestations and approach to treatment of hyperuricemia are summarized.
Hyperuricemia
This document summarizes information about hyperuricemia and uric acid. It discusses that uric acid is produced from the breakdown of purines and defines hyperuricemia. The document outlines the physiology of uric acid production and excretion by the kidneys. It describes some causes of high uric acid levels like Lesch-Nyhan syndrome and gout. The document also discusses hypouricemia and mentions several methods for measuring uric acid levels like chemical, enzymatic, IDMS and HPLC methods. It provides reference ranges and notes some physiological variations in uric acid levels.
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Diabetic kidney disease remains a major global health problem. Recent research has provided insights into the pathophysiology and has identified new diagnostic and therapeutic approaches. Several large clinical trials have shown that sodium-glucose cotransporter-2 inhibitors, glucagon-like peptide-1 receptor agonists, mineralocorticoid receptor antagonists, and endothelin receptor antagonists can reduce kidney disease progression and cardiovascular events in patients with diabetes and kidney disease. Ongoing trials are further evaluating combination therapies and the benefits of these agents in non-diabetic kidney disease and heart failure.
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Dr. Faraz Farishta is a consultant endocrinologist and president of the Diabetes Awareness Foundation. The document discusses hyperuricemia (high levels of uric acid in the blood) and its treatment. It notes that hyperuricemia can be caused by increased uric acid production or decreased excretion. Febuxostat is introduced as a selective xanthine oxidase inhibitor drug that is more effective than allopurinol at lowering uric acid levels. It has advantages over allopurinol such as being safer for use in patients with renal impairment and not requiring dose adjustment in mild to moderate cases.
Gout and Hyperuricemia
Module: Pharmacotherapy III
Module Coordinator: Dr. Arwa M. Amin Mostafa
Academic Level: Postgraduate, Master of Pharmacy in Clinical Pharmacy
School: Dubai Pharmacy College
Year of first presented in Class: 2018
This presentation is for Educational purpose. It has no commercial value associated with it.
Dyslipidemia case study
A 35-year-old male presented with skin lesions on his elbows and knees. Laboratory tests showed high total cholesterol, triglycerides, and blood sugar levels. An ECG also showed T-wave changes. Given the patient's family history of diabetes and early heart disease, further investigations of liver, kidney, thyroid, and cardiac function were recommended. The patient is at risk of complications like heart disease and pancreatitis due to secondary hyperlipidemia, which is most likely caused by an underlying condition like hypothyroidism, obesity, or medication use. Treatment would involve lifestyle changes, diabetes control, lipid-lowering medications, and consultation with cardiology.
Magnesium disorders
Magnesium deficiency can cause a wide variety of features including hypocalcaemia, hypokalaemia and cardiac and neurological manifestations. Chronic low magnesium state has been associated with a number of chronic diseases including diabetes, hypertension, coronary heart disease, and osteoporosis.
Estimation of glomerular filtration rate
Renal function, or glomerular filtration rate (GFR), indicates the state of the kidneys and is measured by the volume of fluid filtered from the glomerular capillaries into the Bowman's capsule per unit of time. GFR can be estimated by measuring creatinine or other substances that are freely filtered but not reabsorbed or secreted by the kidneys. While creatinine clearance is commonly used to estimate GFR, it may overestimate by 10-20% due to minimal creatinine secretion. Alternative methods to more directly measure GFR include collecting urine over 24 hours or injecting inulin, though these have limitations as well.
Gout
1. Gout and pseudogout are types of crystal arthritis caused by sodium urate crystals or calcium pyrophosphate crystals respectively.
2. Gout prevalence is increasing, especially in developed countries, and affects men more than women. Risk factors include diet, medications, age, gender and medical conditions.
3. Pseudogout usually affects the knees and wrists of elderly women, causing painful flare ups that are treated similarly to gout.
Anemia in Chronic Kidney DIsease
Anemia is a common complication of chronic kidney disease that can cause fatigue. While the kidneys normally produce erythropoietin to stimulate red blood cell production, CKD patients have relative erythropoietin deficiency. This leads to anemia which, if left untreated, can negatively impact quality of life and cardiovascular health. Erythropoiesis-stimulating agents and iron supplementation are used to treat anemia in CKD, though the appropriate hemoglobin target level remains an area of ongoing research and debate given risks identified with higher targets in some studies.
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1) Anaemia is common in chronic kidney disease (CKD) due to reduced kidney function and erythropoietin production. It can cause lower quality of life and increased risk of cardiovascular complications.
2) Guidelines recommend diagnosing anaemia of CKD in adults with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73m2 and hemoglobin ≤11 g/dL.
3) Treatment involves iron supplementation and erythropoiesis-stimulating agents (ESAs) to increase hemoglobin levels, with a target range of 11-12 g/dL according to recent guidelines. Higher targets may increase risk without clear benefits.
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AKI, CKD, and ESRD are conditions involving the kidneys. AKI is a sudden loss of kidney function that develops over days or weeks and is often reversible. It is caused by prerenal factors like low blood pressure or intrinsic renal damage. Common causes include sepsis, low fluid intake, and medications. Diagnosis is based on increases in BUN and creatinine and decreased urine output. Treatment focuses on identifying and treating the underlying cause while managing fluid, electrolyte and acid-base imbalances. Long term kidney damage can progress to CKD or end stage renal disease requiring renal replacement therapies.
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Chronic Kidney Disease
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function lasting over 3 months. CKD is evaluated based on glomerular filtration rate (GFR) and markers of kidney damage. Progression is defined as a sustained decline in GFR or a 25% drop from baseline. Management focuses on preventing progression through blood pressure control, ACE inhibitors/ARBs, glycemic control, salt restriction, and lifestyle changes like exercise and smoking cessation. Complications include anemia, bone disease, vitamin D deficiency, acidosis, cardiovascular disease, and increased risk of infection. Dialysis is initiated when symptoms develop or control of volume, pressure, or nutrition cannot be maintained.
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2. AKI is a common complication in ICU patients with mortality rates ranging from 15-60%. Even mild, reversible AKI can have serious clinical consequences.
3. Causes of AKI include pre-renal such as hypovolemia, renal including acute tubular necrosis, and post-renal such as obstruction. Management involves identifying and treating the underlying cause, maintaining hemodynamic stability with fluids and vasopressors, and starting renal replacement therapy for complications.
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The document discusses the relationship between hyperuricemia, chronic kidney disease, and cardiovascular disease. It reviews evidence that higher uric acid levels increase the risk of chronic kidney disease in the general population. However, in patients with chronic kidney disease, hyperuricemia itself was not associated with progression to end-stage renal disease. It was associated with increased risk of cardiovascular events. Treating hyperuricemic chronic kidney disease patients with allopurinol for 9-24 months helped preserve renal function and reduced cardiovascular events.
Fatty liver disease with Diabetes Mellitus [BANGLADESH]
A 52-year-old female with diabetes and hypertension for several years was found to have fatty liver disease based on elevated liver enzymes and ultrasound findings. She had overweight and mild liver enlargement but no signs of cirrhosis. Fatty liver disease is common in people with diabetes and obesity, as excess fat can accumulate in the liver. Lifestyle changes like weight loss and exercise through diet modification are the primary treatments recommended. Medical therapies for diabetes may also help improve fatty liver condition.
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The document discusses purine and pyrimidine metabolism and their role in genetic material replication, transcription, protein synthesis and cellular metabolism. It then focuses on hyperuricemia and gout, explaining that this results from increased uric acid production or impaired excretion. The key biochemical pathways of purine degradation to uric acid are described, as well as the factors influencing uric acid solubility and excretion by the kidneys through specific transporters. The causes, clinical manifestations and approach to treatment of hyperuricemia are summarized.
Hyperuricemia
This document summarizes information about hyperuricemia and uric acid. It discusses that uric acid is produced from the breakdown of purines and defines hyperuricemia. The document outlines the physiology of uric acid production and excretion by the kidneys. It describes some causes of high uric acid levels like Lesch-Nyhan syndrome and gout. The document also discusses hypouricemia and mentions several methods for measuring uric acid levels like chemical, enzymatic, IDMS and HPLC methods. It provides reference ranges and notes some physiological variations in uric acid levels.
Antithyroid drugs and liver thyroalex
This document discusses antithyroid drugs and their potential to cause liver injury. It provides background on the common antithyroid drugs propylthiouracil (PTU) and methimazole, and their uses and side effects. The mechanisms of antithyroid drug-induced liver injury are not fully understood, but may involve reactive metabolites, genetic factors, and immune responses. Factors like age, gender, concomitant medications, and underlying thyroid conditions can also influence the risk of liver injury. Therapeutic strategies discussed include drug cessation, monitoring liver function, and potential protective treatments in experimental models.
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Diabetic kidney disease remains a major global health problem. Recent research has provided insights into the pathophysiology and has identified new diagnostic and therapeutic approaches. Several large clinical trials have shown that sodium-glucose cotransporter-2 inhibitors, glucagon-like peptide-1 receptor agonists, mineralocorticoid receptor antagonists, and endothelin receptor antagonists can reduce kidney disease progression and cardiovascular events in patients with diabetes and kidney disease. Ongoing trials are further evaluating combination therapies and the benefits of these agents in non-diabetic kidney disease and heart failure.
Febuxostat medical slides
Dr. Faraz Farishta is a consultant endocrinologist and president of the Diabetes Awareness Foundation. The document discusses hyperuricemia (high levels of uric acid in the blood) and its treatment. It notes that hyperuricemia can be caused by increased uric acid production or decreased excretion. Febuxostat is introduced as a selective xanthine oxidase inhibitor drug that is more effective than allopurinol at lowering uric acid levels. It has advantages over allopurinol such as being safer for use in patients with renal impairment and not requiring dose adjustment in mild to moderate cases.
Gout and Hyperuricemia
Module: Pharmacotherapy III
Module Coordinator: Dr. Arwa M. Amin Mostafa
Academic Level: Postgraduate, Master of Pharmacy in Clinical Pharmacy
School: Dubai Pharmacy College
Year of first presented in Class: 2018
This presentation is for Educational purpose. It has no commercial value associated with it.
Dyslipidemia case study
A 35-year-old male presented with skin lesions on his elbows and knees. Laboratory tests showed high total cholesterol, triglycerides, and blood sugar levels. An ECG also showed T-wave changes. Given the patient's family history of diabetes and early heart disease, further investigations of liver, kidney, thyroid, and cardiac function were recommended. The patient is at risk of complications like heart disease and pancreatitis due to secondary hyperlipidemia, which is most likely caused by an underlying condition like hypothyroidism, obesity, or medication use. Treatment would involve lifestyle changes, diabetes control, lipid-lowering medications, and consultation with cardiology.
Magnesium disorders
Magnesium deficiency can cause a wide variety of features including hypocalcaemia, hypokalaemia and cardiac and neurological manifestations. Chronic low magnesium state has been associated with a number of chronic diseases including diabetes, hypertension, coronary heart disease, and osteoporosis.
Estimation of glomerular filtration rate
Renal function, or glomerular filtration rate (GFR), indicates the state of the kidneys and is measured by the volume of fluid filtered from the glomerular capillaries into the Bowman's capsule per unit of time. GFR can be estimated by measuring creatinine or other substances that are freely filtered but not reabsorbed or secreted by the kidneys. While creatinine clearance is commonly used to estimate GFR, it may overestimate by 10-20% due to minimal creatinine secretion. Alternative methods to more directly measure GFR include collecting urine over 24 hours or injecting inulin, though these have limitations as well.
Gout
1. Gout and pseudogout are types of crystal arthritis caused by sodium urate crystals or calcium pyrophosphate crystals respectively.
2. Gout prevalence is increasing, especially in developed countries, and affects men more than women. Risk factors include diet, medications, age, gender and medical conditions.
3. Pseudogout usually affects the knees and wrists of elderly women, causing painful flare ups that are treated similarly to gout.
Anemia in Chronic Kidney DIsease
Anemia is a common complication of chronic kidney disease that can cause fatigue. While the kidneys normally produce erythropoietin to stimulate red blood cell production, CKD patients have relative erythropoietin deficiency. This leads to anemia which, if left untreated, can negatively impact quality of life and cardiovascular health. Erythropoiesis-stimulating agents and iron supplementation are used to treat anemia in CKD, though the appropriate hemoglobin target level remains an area of ongoing research and debate given risks identified with higher targets in some studies.
Anaemia of chronic kidney disease GUIDELINES TO PRACTICE 2013
1) Anaemia is common in chronic kidney disease (CKD) due to reduced kidney function and erythropoietin production. It can cause lower quality of life and increased risk of cardiovascular complications.
2) Guidelines recommend diagnosing anaemia of CKD in adults with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73m2 and hemoglobin ≤11 g/dL.
3) Treatment involves iron supplementation and erythropoiesis-stimulating agents (ESAs) to increase hemoglobin levels, with a target range of 11-12 g/dL according to recent guidelines. Higher targets may increase risk without clear benefits.
Kidney diseases by Harrison Mbohe
AKI, CKD, and ESRD are conditions involving the kidneys. AKI is a sudden loss of kidney function that develops over days or weeks and is often reversible. It is caused by prerenal factors like low blood pressure or intrinsic renal damage. Common causes include sepsis, low fluid intake, and medications. Diagnosis is based on increases in BUN and creatinine and decreased urine output. Treatment focuses on identifying and treating the underlying cause while managing fluid, electrolyte and acid-base imbalances. Long term kidney damage can progress to CKD or end stage renal disease requiring renal replacement therapies.
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Alcoholic liver disease is a result of over-consuming alcohol that damages the liver, leading to a buildup of fats, inflammation, and scarring. It can be fatal.
Ckd mbd
Chronic kidney disease-mineral bone disorder (CKD-MBD) is a common complication in chronic kidney disease caused by reduced kidney function and mineral metabolism abnormalities. This leads to high phosphate, activation of parathyroid hormone, and bone abnormalities from renal osteodystrophy to vascular calcification. Treatment focuses on controlling phosphate levels through binders like sevelamer and cinacalcet to reduce parathyroid hormone in order to prevent bone disease and fractures while minimizing cardiovascular risks.
Hif ph inhibitors for anemia in ckd
HIF PH inhibitors stabilize HIF and stimulate endogenous EPO production, facilitating erythropoiesis and improving iron metabolism in CKD patients. Compared to ESAs, HIF PH inhibitors maintain physiological EPO levels, decrease cardiovascular risks, and reduce need for rescue therapies like transfusions. By coordinating EPO production, iron transport, and hepcidin inhibition, HIF PH inhibitors provide a targeted approach to anemia in CKD.
Diabetic nephropathy
Diabetic nephropathy is a chronic kidney disease characterized by gradually increasing urinary albumin excretion, high blood pressure, declining kidney function, and presence of diabetic retinopathy. It develops in 20-40% of people with diabetes and is the leading cause of end-stage renal disease. The pathophysiology involves metabolic and hemodynamic pathways as well as genetic factors. Hyperglycemia causes kidney damage through increased polyol pathway flux, formation of advanced glycation end products, activation of protein kinase C, and other mechanisms. Hemodynamic changes from hypertension increase glomerular pressure and permeability. Genetic factors like ACE polymorphisms also influence risk. Progression is associated with proteinuria, anemia
alcoholoc liver disease
Alcohol consumption can lead to various liver diseases known as alcoholic liver disease (ALD). Chronic heavy drinking is responsible for 50% of chronic liver disease cases in India. Symptoms of ALD may not appear until the disease is advanced and include fatigue, abdominal swelling and pain, and jaundice. Alcohol is metabolized in the liver, producing reactive oxygen species that can cause oxidative stress, fatty liver, inflammation, fibrosis and eventually cirrhosis over many years. Diagnosis involves assessing drinking history, symptoms, lab tests and biopsy. Treatment focuses on abstaining from alcohol. Corticosteroids and antioxidants may help in some cases. Liver transplantation is an option for end-stage ALD but is not usually recommended for
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Similar to Hyperuricemia ; Focus on Treatment
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Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function lasting over 3 months. CKD is evaluated based on glomerular filtration rate (GFR) and markers of kidney damage. Progression is defined as a sustained decline in GFR or a 25% drop from baseline. Management focuses on preventing progression through blood pressure control, ACE inhibitors/ARBs, glycemic control, salt restriction, and lifestyle changes like exercise and smoking cessation. Complications include anemia, bone disease, vitamin D deficiency, acidosis, cardiovascular disease, and increased risk of infection. Dialysis is initiated when symptoms develop or control of volume, pressure, or nutrition cannot be maintained.
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2. AKI is a common complication in ICU patients with mortality rates ranging from 15-60%. Even mild, reversible AKI can have serious clinical consequences.
3. Causes of AKI include pre-renal such as hypovolemia, renal including acute tubular necrosis, and post-renal such as obstruction. Management involves identifying and treating the underlying cause, maintaining hemodynamic stability with fluids and vasopressors, and starting renal replacement therapy for complications.
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- Considering aspirin and dual antiplatelet therapy for some patients based on cardiovascular risk factors.
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2. Treatment strategies for chronic kidney disease including screening for risk factors, slowing disease progression through treatment of comorbid conditions, and preparing for renal replacement therapies like dialysis and transplant as kidney function declines.
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Diabetic nephropathy is a clinical syndrome characterized by the following :
Persistent albuminuria (>300 mg/d or >200 μg/min) that is confirmed on at least 2 occasions 3-6 months apart.
Progressive decline in the glomerular filtration rate (GFR).
Elevated arterial blood pressure.
Three major histologic changes occur in the glomeruli of persons with diabetic nephropathy:
First, mesangial expansion is directly induced by hyperglycemia, perhaps via increased matrix production or glycation of matrix proteins.
Second, thickening of the glomerular basement membrane (GBM) occurs.
Third, glomerular sclerosis caused by intraglomerular hypertension (induced by dilatation of the afferent renal artery or from ischemic injury induced by hyaline narrowing of the vessels supplying the glomeruli).
These different histologic patterns appear to have similar prognostic significance.
Several issues are key in the medical care of patients with diabetic nephropathy.
These include glycemic control, management of hypertension, and reducing dietary salt intake and phosphorus and potassium restriction in advanced cases.
A meta-analysis from the Cochrane Database shows a large fall in blood pressure with salt restriction, similar to that of single-drug therapy
Ueda 2016 7-diabetic complications - adel el sayed
This document discusses nephropathy (kidney damage) in patients with type 2 diabetes. It recommends screening all patients with type 2 diabetes for kidney damage at diagnosis and annually thereafter. For those found to have microalbuminuria, the document recommends repeating a urine test several times to confirm and then monitoring regularly. It provides referral criteria to specialists for patients with more advanced kidney disease. Treatment recommendations include ACE inhibitors or ARBs for micro- or macroalbuminuria and intensive control of blood pressure and blood glucose to protect kidney function.
Management of Hypertension in Diabetic Patients with Chronic Kidney Disease: ...
Diabetes is associated with markedly increased cardiovascular risk, a risk compounded with imposition of chronic kidney disease (CKD). More than 80% of people with diabetes and CKD have hypertension, and many have an obliterated nocturnal blood pressure “dip,” the normal physiological drop in blood pressure during sleep. Appropriate blood pressure measurement is the Achilles heel of hypertension management, especially in diabetic kidney disease (DKD).
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- Diabetic kidney disease is a major cause of mortality and morbidity in patients with diabetes. It can progress from microalbuminuria to macroalbuminuria and decreased kidney function over many years.
- Risk factors include uncontrolled hypertension and hyperglycemia, genetics, obesity, and smoking. The pathogenesis involves hemodynamic changes, activation of metabolic pathways, growth factors, the renin-angiotensin system, and oxidative stress.
- Management involves tight glycemic and blood pressure control, lifestyle modifications like diet and exercise, and medications targeting glucose, blood pressure, lipids, and proteinuria. Dialysis and kidney transplantation are treatment options for end-stage kidney disease.
Ckd dr. shanjida
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CKD Dr. Shanjida
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Chapter 6 Endocrine disorders by Dr. Derejepdf
Chronic kidney disease (CKD) is common in patients with diabetes and is diagnosed through elevated albuminuria and reduced estimated glomerular filtration rate (eGFR). CKD attributed to diabetes occurs in 20-40% of patients and can progress to end-stage renal disease requiring dialysis. Diabetic retinopathy, caused by chronic hyperglycemia, is the most common cause of blindness and is assessed through eye exams. Neuropathy is assessed through history and examination of sensation, with annual 10-g monofilament testing to check for high-risk feet. Foot care includes inspection, assessment of deformities and pulses, and referral for ongoing surveillance in high-risk patients to prevent ulcers and amputations.
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Management of Hypertension in Diabetic Patients with Chronic Kidney Disease: ...
Management of Hypertension in Diabetic Patients with Chronic Kidney Disease: ...
Ueda 2016 7-diabetic complications - adel el sayed
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Management of Hypertension in Diabetic Patients with Chronic Kidney Disease: ...
Management of Hypertension in Diabetic Patients with Chronic Kidney Disease: ...
Pediatric Type 2 Diabetes Mellitus. BY DR SAYED ISMAIL
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Hyperuricemia ; Focus on Treatment
- 1. HYPERURICEMIA Focus onTreatment AdeWijaya, MD – February 2018
- 2. Introduction ■ Overproduction or under-excretion of uric acid, a product of purine catabolism physiologically excreted in the urine ■ Closely related to cardiovascular and renal complications ■ Gout
- 3. When to treat ? ■ Two or more acute gout attacks per year, ■ Presence of tophi, ■ Chronic kidney disease (CKD) stage 2 or more, ■ Presence of renal stones, Target < 6 mg/dL
- 6. Key recommendations for the management of hyperuricemia A careful management of chronic hyperuricemia • Correct education of patients to improve adherence and optimize the results • Modifiable risk factors: • Obesity (Weight loss and restriction of dietary purines) • Reduce/abolish beer, sodas, spirits, and fructose-rich beverages consumption • Increase the intake of vitamin c • Reduce or stop Loop and thiazide diuretics therapy • SUA levels should be under the target value of 7 mg/dL • Assess the global cardiovascular risk of patients with elevated SUA levels • Urate lowering therapies with XO inhibitors should be prescribed as soon as the diagnosis is made
- 7. Allopurinol dose: ■ The daily dose of allopurinol recommended for reaching target values of uricemia is 100–600 mg, although sometimes it must be up to 900 mg in patients without impaired renal function ■ A higher dosage of allopurinol (300 mg twice daily) has resulted in quality improvement of vascular biology and left ventricular hypertrophy ■ In obese or hypertensive adolescents, the dosage of allopurinol administered was 200 mg twice daily ■ Fatal hypersensitivity reaction
- 8. Summary ■ A multifactorial pathological condition ■ Closely related to CVD and renal incident development ■ Improve endothelial function at higher dose ■ Target < 6 mg/dL
- 9. References ■ Gliozzi, M., Malara, N., Muscoli, S., & Mollace,V. (2016).The treatment of hyperuricemia. International journal of cardiology,213, 23-27. ■ Bove, M., Cicero,A. F. G.,Veronesi, M., & Borghi,C. (2017).An evidence-based review on urate-lowering treatments: implications for optimal treatment of chronic hyperuricemia.Vascular health and risk management, 13, 23. ■ Sattui, S. E., & Gaffo,A. L. (2016).Treatment of hyperuricemia in gout: current therapeutic options, latest developments and clinical implications. Therapeutic advances in musculoskeletal disease, 8(4), 145-159.