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Chronic Kidney Disease PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Chronic Kidney Disease” by Sumit Kumar, MD, MPH.

This medical PowerPoint presentation is about Chronic Kidney Disease (CKD), a long-term condition in which the kidneys gradually lose their ability to filter waste products from the blood. It is also known as chronic renal disease. The disease typically progresses slowly over months or years, and it can eventually lead to kidney failure.

The primary function of the kidneys is to filter waste and excess fluids from the blood, which are then excreted in the urine. When the kidneys become damaged, waste products build up in the blood, leading to a range of complications.

There are various causes of CKD, including high blood pressure, diabetes, and certain genetic conditions. Other risk factors include smoking, obesity, and a family history of kidney disease.

Symptoms of CKD can include fatigue, nausea, loss of appetite, swollen ankles, and difficulty sleeping. However, in the early stages of the disease, there may be no noticeable symptoms.

Treatment for CKD depends on the underlying cause and the severity of the condition. In some cases, medication and lifestyle changes may be sufficient to slow the progression of the disease. In more advanced cases, dialysis or kidney transplantation may be necessary.

Preventing CKD involves managing risk factors such as maintaining a healthy weight, managing blood pressure and blood sugar levels, and avoiding smoking. Regular check-ups with a healthcare provider can also help detect the disease early.

Tags : Chronic Kidney Disease, CKD, chronic renal disease, Nephrology, Nephrology PowerPoint presentation

Published on : Jun 07, 2023 | Views : 953 | Downloads : 7

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Slide 1-

Chronic Kidney Disease Sumit Kumar, MD, MPH Presbyterian Hospital, Dallas, TX
Slide 2-

The Story of Mr. George Lopez 45 yr HM with Diabetes for 10 yrs, “reasonably well controlled” PMH: Hypertension for 7 yrs..well controlled BMI of 30 Dyslipidemia Fam Hx: Diabetes; Soc Hx: Sedentary; non smoker; Comedian Exam 139/85 – Mild Obesity, rest fairly normal Labs BUN 28, Creatinine 1.8, Urine protein (dipstick) 2+
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Chronic Kidney Disease Definition Chronic, irreversible loss of kidney function attributable to loss of functional nephron mass – pathophysiologic processes for more than 3 months.
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Pathophysiology of CKD Final Common Pathway is loss of nephron mass Mediated by vasoactive molecules, cytokines and growth factors, renin angiotensin axis Diabetes Hypertension Chronic GN Cystic Disease Tubulointerstitial disease
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Estimation of GFR Modification of Diet in Renal Disease (MDRD) Formula Estimated GFR = 1.86 (Serum Creat) -1.154 X (age) -0.203 Multiply by 0.742 for women Multiply by 1.21 for African Americans Cockroft Gault Formula (140 – age) X Body Weight (Kg) 72 X Serum Creatinine (mg/dL) Multiply by 0.85 for women
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Staging of Chronic Kidney Disease
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Who is at Risk for CKD? Family history of heritable renal disease Diabetes Hypertension Auto-immune disease Old age Prior episode of ARF Current evidence of renal damage, even with normal or increased GFR
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MDRD GFR for Mr Lopez Diabetic, Hypertension, Metabolic Syndrome X Stage 3 CKD GFR = 44 ml/min/1.73 m2
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Etiology and Epidemiology 6% of the US population has CKD (Stage 1 and 2) Additional 4-5% have Stage 3 and 4 CKD Diabetic nephropathy Hypertension – chronic ischemic nephropathy Very high CV disease burden
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Monitoring of CKD Serial measurements of Creatinine GFR Albumin Albumin-creatinine ratio in the 1st morning sample Electrolytes including HCO3, Ca, Phos; alkaline phosphatase, iron studies, intact PTH Renal sonogram Renal biopsy
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Symptoms of CKD Stage 1 and 2 Asymptomatic, hypertension Stage 3 and 4 Anemia – loss of energy Decreasing appetite; poor nutrition Abnormalities in Calcium, Phosphorus metabolism Sodium, water, potassium and acid base abnormalities Stage 5 All of the above – accentuated; eventually overt uremia
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Estimates of Subgroups at Increased Risk for CKD
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1992-93 1997-98 2002-03 Steady Rise in the Rate of CKD in Medicare population over the last decade
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Common Causes and Presentation
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Genetic Considerations Autosomal dominant PKD Alport’s hereditary nephritis Familial FSGS Nephronopthisis Medullary cystic kidney disease Fabry’s disease
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Natural History of CKD Most CKD has a logarithmic progression and is predictable
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Mr. Lopez – Progressive Decline
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Clinical Features of Diabetic CKD
Slide 26-

Clinical Features of Non-Diabetic CKD
Slide 27-

Pathophysiology of Uremia Azotemia – refers to the retention of nitrogenous waste products. Uremia – advanced stages of azotemia with end organ dysfunction Accumulation of products of protein metabolism Urea – anorexia, malaise, vomiting and headaches Loss of other renal functions Erythropoietin deficiency – anemia Metabolic bone disease; endocrine abnormalities Fluid, electrolyte and acid base disorders
Slide 28-

Symptoms of Uremia
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Sodium and water Imbalance Glomerulotubular feedback is disrupted – sodium retention, contributes to hypertension; hyponatremia is unusual. Higher than usual doses for diuretics. In situations with volume depletion – can be severe, because of inadequate sodium retention. Treatment: Salt restriction; high doses of diuretics
Slide 30-

Potassium Imbalance Potassium GI excretion is augmented Constipation, dietary intake, protein catabolism, hemolysis, hemorrhage, transfusion of stored blood, metabolic acidosis, Drugs: ACE inhibitors, ARBs, B blockers, K sparing diuretics and NSAIDs Hyporeninemic hypoaldosteronism: Diabetes, sickle cell disease
Slide 31-

Acid Base Imbalance Damaged kidneys are unable to excrete the 1 mEq/kg/d of acid generated by metabolism of dietary proteins. NH3 production is limited because of loss of nephron mass Decreased filtration of titrable acids – sulfates, phosphates Decreased proximal tubular bicarb reabsorption, decreased positive H ion secretion Arterial pH: 7.33 - 7.37; serum HCO3 rarely below 15 – buffering offered by bone calcium carbonate and phosphate Should be maintained over 21 Treatment: Sodium bicarbonate, calcium carbonate, sodium citrate
Slide 32-

Bone Disease
Slide 33-

Treatment of Secondary Hyperparathyroidism Phosphorus control in diet Phosphate binders Calcium acetate (Phoslo), calcium carbonate (TUMS), sevelamer (Renagel) , lanthanum (Fosrenol) Oral Vitamin D Calcimemetic agent: Cinacalcet (Sensipar)
Slide 34-

Mineral Metabolism Calciphylaxis Calcemic uremic arteriopathy Extraosseous/metastatic calcification of soft tissues and blood vessels Devastating complication Treatment: controversial Sodium thiosulfate Parathyroidectomy
Slide 35-

Cardiovascular Abnormalities Leading cause of morbidity and mortality in patients with CKD at all stages Ischemic CAD Hypertension and LVH Congestive heart failure Uremic pericarditis
Slide 36-

Trends in the interactions of diabetes, congestive heart failure, & CKD: 2002-2003 LVH and dilated CM are the most ominous risk factors for excess mortality and morbidity High cardiac output Extracellular fluid overloa AV shunt Anemia Medicare: general Medicare CKD patients continuously enrolled in Medicare Parts A & B for two consecutive years (numbers estimated from 5 percent sample)
Slide 37-

Cardiac Complications
Slide 38-

Hematological Abnormalities Anemia Chronic blood loss, hemolysis, marrow suppression by uremic factors, and reduced renal production of EPO Normocytic, normochromic Rx: Iron and Epo as needed Coagulopathy Mainly platelet dysfunction – decreased activity of platelet factor III, abnormal platelet aggregation and adhesiveness and impaired thrombin consumption Increased propensity to bleed – post surgical, GI Tract, pericardial sac, intracranial Increased thrombotic tendency – nephrotic syndrome
Slide 39-

Other Abnormalities Neuromuscular Central, peripheral and autonomic neuropathy Peripheral Sensory/Motor Neuropathy Stage 4 for more than 6 months Restless leg syndrome Gastrointestinal Uremic fetor Gastritis, peptic disease, mucosal ulcerations, AVMs Endocrine Glucose metabolism Estrogen levels – amenorrhea, frequent abortions Male: oligospermia, germinal cell dysplasia, delayed sexual maturation Dermatologic Pallor, ecchymoses, hematomas, calciphylaxis, pruritus, uremic frost
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Uremic Complications
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Therapeutics in CKD Non Pharmacologic Risk Factor Modification Pharmacologic Treatment of complications
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Therapeutics in CKD Non Pharmacologic Risk Factor Modification Pharmacologic Treatment of complications
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Therapeutics in CKD Non Pharmacologic Risk Factor Modification Pharmacologic Treatment of complications
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