case presentation on CKD
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This document presents a case study of a 50-year-old male patient with chronic kidney disease due to diabetic nephropathy. The patient has a 15-year history of type 2 diabetes and non-proliferative diabetic retinopathy. Diagnostic tests show elevated blood sugar, creatinine, and signs of kidney damage. The patient is assessed as having progressed chronic kidney disease due to diabetic nephropathy. His treatment plan includes insulin, medications to protect the kidneys and manage symptoms, and lifestyle changes to control his diabetes and slow disease progression.
case presentation on CKD
- 1. CASE PRESENTATION ON CHRONIC KIDNEY DISEASE WITH DIABETIC NEPHROPATHY Presented By Percy Arpitha.B Pharm-D IIIYr 12Y01T0019 1
- 2. DEMOGRAPHIC DATA NAME: xxx AGE: 50 yrs GENDER: male I.P. NO: 8998/14 D.O.A: 8-1-14 D.O.D: Not Known WARD: Delux Ward CONSULTANT: Dr. V. Venkata Ranga Reddy REFERRED TO : Dr. Nemali Ravi Kumar Reddy Dr. Venkata Pakkir Reddy 2
- 3. SUBJECTIVE 3
- 4. CHIEF COMPLAINTS C/O loss of appetite( anorexia) since a month C/O Generalized weakness & fatigue HISTORY OF PRESENT ILLNESS H/O fever (night time) since 15 days 4
- 5. PAST MEDICAL HISTORY: Type II diabetes mellitus(DM) since 15 yrs and not on regular medication NPDR(Non Proliferative Diabetic Retinopathy) PAST MEDICATION HISTORY: not known PAST SURGICAL HISTORY: Nil 5
- 6. PERSONAL HISTORY AND HABITS: Chronic smoker and alcoholic since 20yrs FAMILY HISTORY: Father suffered with DM & HTN 6
- 7. OBJECTIVE 7
- 8. GENERAL EXAMINATION PHYSICALEXAMINATION Date 8-1-15 9-1-15 10-1-15 Temp N N N B.P in mm of Hg 120/80 140/90 110/70 P.R 92/min 86/min 86/min R.R 24/min 22/min 24/min SYSTEMEXAMINATION Cvs: s1,s2 + Rs: ↓↓ breath sounds (dull note) 8
- 9. DIAGNOSTIC INVESTIGATIONS COMPLETE BLOOD PICTURE TEST TEST VALUE NORMAL VALUE Hb 10 g/dl 13-17g/dl RBC 3.79 million/cumm 4.5-5.5million/cumm TLC(WBC) 15600 cells/cumm 4000- 11000cells/cumm Differential Leukocyte Count Neutrophils 89 % 40-80% Lymphocytes 08 % 20-40% Eosinophils 01 % 0-6% Monocytes 02 % 2-10% ESR 38 mm/hr 0-20mm/hr 9
- 10. TEST TEST VALUE NORMAL VALUE TOTAL BILIRUBIN 0.7 mg/dl 0.0-1.0mg/dl DIRECT BILIRUBIN 0.2 mg/dl 0.0-0.25mg/dl INDIRECT BILIRUBIN O.5 mg/dl 0.3-1.0 mg/dl SGPT 55 IU/L 0-45 IU/L SGOT 23 IU/L 0-40 IU/L ALKALINE PHOSPHATASE 222 IU/L 30-170 IU/L TOTAL PROTEIN 7.8 g/dl 6-8g/dl ALBUMIN 3.0 g/dl 3.5-5.5g/dl GLOBULIN 4.8 g/dl 2.3-3.6g/dl LIVER FUNCTION TESTS 10
- 11. TEST 8-1-15 9-1-15 10-1-15 NORMAL VALUE FASTING 240 mg/dl 210 mg/dl 60-110mg/dl RANDOM 255 mg/dl 315 mg/dl 80-150mg/dl BLOOD SUGAR TEST RENAL FUNCTION TESTS TEST 8-1-15 9-1-15 Normal value BUN 67 mg/dl 10-50mg/dl Creatinine 1.8 mg/dl 1.9 mg/dl 0.6-1.6mg/dl 11
- 12. URINE ANALYSIS Color : Light yellow Reaction : Acidic Albumin : Traces Sugar : ++(two plus) Deposit cells : 4-5 pus cells/HPF 3-4 epithelial cells/HPF Casts : Nil Crystals : Nil Ketone : -ve RBC : -ve 12
- 13. ELECTROLYTES TEST 9-1-15 Normal value Sodium 139 135-145 mEq/l Chloride 105 98-105 mEq/l Potassium 5.2 3.5-5.5 mEq/l Calcium 9.0 9-11 mg/dl 13
- 14. X-ray Chest PA View Impression : normal CPB Peripheral Smear WBC : Neutrophillic leucocytosis RBC : Normocytic hypochromic with mild anisocytosis PLATELETS : Mild thrombocytosis Impression: normocytic normochromic anemia with neutrophillic leucocytosis 14
- 15. ASSESMENT 15
- 16. Based On Subjective And Objective Evidence The Patient Is A Known Case Of Diabetes Mellitus And Newly Diagnosed To Have Progressed Chronic Kidney Disease Due To Diabetic Nephropathy 16
- 17. PLANNING 17
- 18. S.N O BRANDNAME GENERICNAME DOSE ROA FREQUEN CY DATE BEGIN DATEEND 1 Inj. Rabeloc RABEPRAZOLE 20mg IV OD 8-1-15 NotKnown 2 Inj. Humanmixtard INSULIN(Shortacting+ longacting) 24 U S/C BD 9-1-15 NotKnown 3 Tab.Renosave N-Acetylcysteine-150mg+Taurine-500mg 1 tab Oral OD 8-1-15 NotKnown 5 Tab.Supradyn MULTI VITAMIN& MULTI MINERAL SUPPLEMENT 1 tab Oral OD 9-1-15 NotKnown 6 Syp.Aristozyme PEPSIN-10mg/5ml+ FUNGAL DIASTASE-50mg 5ml Oral TID 8-1-15 NotKnown 7 Inj.Emeset ONDENSETRON 2mg/2m l IV BD 10-1-15 NotKnown 18
- 19. DISEASE DISCUSSION DIABETIC NEPHROPATHY Microvascular complication Progressive kidney disease Angiopathy of capillaries 19
- 20. EPIDEMIOLOGY Over 40% of new cases of end-stage renal disease (ESRD) are attributed to diabetes. In 2001, 41,312 people with diabetes began treatment for end-stage renal disease. In 2001, it cost $22.8 billion in public and private funds to treat patients with kidney failure. Minorities experience higher than average rates of nephropathy and kidney disease 20
- 21. PATHOPHYSIOLOGY Three major histologic changes occur in the glomeruli of persons with diabetic nephropathy. 1. Mesangial cell expansion directly induced by hyperglycemia 2. Thickening of the glomerular basement membrane 3. Glomerular sclerosis is caused by intraglomerular hypertension 21
- 22. Uncontrolled diabetes leading to persistent Hyperglycemia induces , Endothelial NO uncoupling Activation of Pkc Formation of advanced glycation end products Activation of polyol pathway 22
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- 28. GLOMERULOSCLEROSIS -Hardening of glomerulus due to scarring -Disturbs filtering process -2 types • Focal segmental • Nodular (significant in diabetes) -Nodules of pink hyaline material formed in glomerular capillary loops 28
- 29. CLINICAL PRESENTATION You may not experience any symptoms until your kidney disease progresses to ESRD. Symptoms of ESRD may include: Microalbuminuria -First laboratory finding of DN -Moderate increase in level of urine albumin -Occurs when kidney leaks small amount of albumin into urine Anorexia Nausea and vomiting General ill feeling Fatigue Headache Itchy and dry skin Swelling of arms and legs 29
- 30. Chronic Kidney Disease (CKD) Or Chronic Renal Failure(CRF) DEFINITION Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss in renal function over a period of time. The three most common causes of CKD are, -Diabetes mellitus -Hypertension and -Glomerulonephritis. Together, these cause about 75% of all adult cases. 30
- 31. 31 PATHOPHYSIOLOGY Involves 2 broad sets of mechanisms Initiating mechanisms specific to underlying etiology Progressive mechanisms, involving hyperfiltration and hypertrophy of viable nephrons
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- 33. 33 Endocrine-metabolic disturbances 2ᵒ hyperparathyroidism Vitamin-D deficient osteomalacia Hypertriglyceridemia CVS and Pulmonary disturbances HTN CHF Pericarditis Pulmonary edema Accelerated atherosclerosis Hematological & Immuological disturbances Anemia Lymphocytopenia Platelet disorders Fluid & electrolyte disturbances Hyponatremia Hyperkalemia Hypophosphatemia Dermatological disturbances Pallor Pruritus GIT disturbances Anorexia Nausea &vomiting Peritonitis Ulceration Neuromuscular disturbances Fatigue Sleep disorders Seizures Coma CLINICAL PRESENTATION
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- 35. 35 COMPLICATIONS Cardiovascular complications -Hypertension -Coronary artery disease -Heart failure -Pericarditis Disorders of mineral metabolism Hematological complications -Anemia -Coagulopathy Hyperkalemia Acid-base disorders Neurologic complications Endocrine disorders
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- 37. 37 Complications Related To Case Uremic pericarditis o Results frominflammationof visceral & parietal membranes of the pericardialsac. o There is a correlation b/wdegree of azotemia(BUNis usually>60)althoughpathogenesis is poorlyunderstood Emphysematous pyelonephritis(EPN) o Severe infection of renal parenchymathat causes gas accumulation in the tissues. o However UTI’sare common in persons withdiabetes, but not all of these infections lead to EPN o Factors predisposing to EPN -Uncontrolled diabetes -High levels of glycated Hb -Impaired host immune mechanism
- 38. 38 Typical presenting features of EPN include thefollowing: • Fever (79%) • Abdominal or flankpain(71%) • Nausea and vomiting (17%) • Dyspnea (13%) • Acute renal impairment (35%) • Alteredsensorium(19%) • Shock(29% Laboratory findings include the following: • Leukocytosis with a left shift • Pyuria
- 39. 39 TREATMENT SLOWING PROGRESSION Treatment of underlying cause Glycemic targets need to be relaxed Blood pressure control is vital. Agents that block RAAS are imp in proteinuric disease Oral alkali therapy in slowing CKD progression if acidemia is present Modify Loading And Maintenance Doses Of Drugs That Are Excreted Through Renal Route.
- 40. 40 NON PHARMACOLOGICAL Dietary management Protein restriction : Decrease protein intake to 0.6-0.8g/kg/day in patients with GFR <30ml/min Phosphate restriction : Food like cola beverages,nuts,beans,meat should be limited.To reduce soft tissue calcification (avoid milk, egg) Salt & water restriction : Moderate sodium restriction to control BP and edema Potassium restriction : If CKD is moderate to severe (avoid food like banana,citrus,coconut water, papaya etc.)
- 41. 41 o Smoking and alcohol cessation o Diet and weight management o Regular exercise PHARMACOLOGICAL o Target BP in both diabetic and non-diabetic patients is <140/90 mm of Hg and in patients with urine albumin excretion >/=30mg/24hrs,target BP is consistently <130/80mm of Hg Tab.Furosemide 40-160mg/day or Tab.Amlodipine 5-20mg/day or Tab.Atnelol 50-100mg/day (contraindicated if concomitant cardiomyopathy with failure. o In both diabetic and non diabetics with albuminuria >300mg/24hrs – ACE inhibitor/ARB with or without a diuretic is preferred.
- 42. 42 Treatment Of ESRD When GFR declines to 5-10ml/min with or without uremic symptoms Renal Replacement Therapy • Hemodialysis • Peritoneal dialysis • Kidney transplantation Pancreatic Transplantation can produce insulin independence which slow or reverse microvascular disease Medical Management
- 43. 43 Treatment Of Pericarditis • Uremic pericarditis is an absolute indication for initiation of dialysis. • Heparin-free dialysate should be used. Treatment Of Anemia • Look for common aggravating causes of anemia eg: GI blood loss, iron deficiency and chronic infections & treat accordingly. • Iron supplementation to ensure adequate response to EPO • Inj.EPO s/c 80-120units/k/week(divided into 2-3 times a week) • The target Hb should be 10-12g/dl
- 44. 44 Monitoring And Interventions Treatment with metformin should be withdrawn when creatinine is ↑ than 1.7mg/dl.This increases lactic acidosis Long acting sulphonyl urea's are replaced by short acting which are metabolised rather than excreted Monitor dosing of renally eliminated drugs Drug toxicity may develop as renal clearence worsens;in particular ,since insulin is renally cleared ,hypoglycemia may develop& can be life theatening in patients with diabetes
- 45. 45 In DN for reducing arterial HTN - In type I DM - ACE inhibitors provide greater benefit -In type II DM – ARB’s shows same effect • But these cause hyperkalemia and renal artery stenosis sometimes hence Non dihydropyridine ca+2 antagonists (diltiazem, verapamil)are suitable alternatives.
- 46. 46 Reference 1.Aminoff.M.J,Andreadis.L.B,Barbour.D.M,Baron.R.B,Barrows.K,B ashore.T.M,et.al.53rded.Current Medical diagnosis and Treatment.2014 2.Fauci.S.A,Kasper.D.L,Longo.D.L,Braunwald.E,Hauser.S.L,Jameso n.J.L et.al.17th ed.USA:Mc Graw Hill companies;2008. 3.Colledge.N.R,Walker.B.R,Raltson.S.H.Davidsons principles and practice of medicine.21st ed.US:elsevier;2010.
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