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Approach to the patient with chronic kidney disease

Approach to the patient with chronic kidney disease. Gülçin Kantarcı, M.D. Nephrology Department. Learning objectives and training goals of this lecture. Define chronic kidney disease. Explain the pathophysiology of chronic kidney disease.

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Approach to the patient with chronic kidney disease

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  1. Approachtothepatientwithchronickidneydisease Gülçin Kantarcı, M.D. Nephrology Department

  2. Learning objectivesandtraininggoals of thislecture • Define chronic kidney disease. • Explain the pathophysiology of chronic kidney disease. • Describe the clinical findings of chronic kidney disease. • Take preventive measures against the development of chronic kidney disease. • List the possible etiology of chronic kidney disease and make a differential diagnosis. • Arrange the initial treatments and refer to a specialist.

  3. REFERENCE &SUGGESTED READING • Current Medical Diagnosis and Treatment, Maxine A. Papadakis, Stephen J. McPhee, Eds. Michael W. Rabow, Associate Ed. http://accessmedicine.com Chapter 22. Kidney Disease • http://www.uptodate.com .(Definition and staging of chronic kidney disease in adults, Screening for chronic kidney disease, Epidemiology of chronic kidney disease)

  4. chronicrenaldiseases (CKD) • CKD is defined as abnormalities of kidney structure or function, present for ≥3 months, with implications for health

  5. Criteriafor CKD KDOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification 2012

  6. Staging of CKD KDOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification 2012

  7. DIAGNOSIS OF CKD •  GFR • Serum creatinine (musclemass, dietarymeatintake, simetidin, trimetoprim) • CreatinineClearance = Ucr x V P cr • Cockcroftformula= 140-age 72 x P cr • EstimatedCrCl (MDRD Study) 1440 x Body weight (women x 0.85)

  8. GFR = 141 X min(Scr/κ,1)α X max(Scr/κ,1)-1.209 X 0.993Age X 1.018 [if female] X 1.159 (if black) CKD-EPI • The CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) equation was developed in an effort to create a formula more precise than the MDRD formula, especially when actual GFR is > 60 mL/min per 1.73 m2. Researchers pooled data from multiple studies to develop and validate this new equation. • The CKD-EPI equation performed better than the MDRD (Modification of Diet in Renal Disease Study) equation, especially at higher GFR, with less bias and greater accuracy.

  9. CKD Symptoms • In the early stages, CKD is asymptomatic. Symptoms develop slowly with the progressive decline in GFR, are nonspecific, and do not manifest until kidney disease is far advanced (GFR < 10–15 mL/min/1.73 m2). • General symptoms of uremia may include fatigue and weakness; anorexia, nausea, vomiting, and a metallic taste in the mouth are also common. Patients or family members may report irritability, difficulty in concentrating, insomnia, restless legs, paresthesias, and twitching. Generalized pruritus without rash may occur.

  10. GFR  35-50% of normal  symptom-free BUN and Cr. levels Normal renal functions maintained *endocrine *excretory *regulatory GFR  20-35% of normal  azotemia still asymptomatic GFR  < 20% of normal  overt renal failure UREMIC SYNDROME

  11. UremicSyndrome • Renalexcretoryfailure • Uremia • Hyperkalemia • Renalendocrinefailure • Anemia • Renalosteodystrophy • Renalmetabolicfailure & acidosis

  12. ClinicalAbnormalities in Uremia • The most common physical finding in CKD is hypertension. • It is often present in early stages of CKD and tends to worsen with CKD progression as sodium excretion is impaired. • In later stages of CKD, this sodium retention may lead to typical physical signs of volume overload. • Fluid & electrolytedisturbances • Acid-Base disorders • Cardiovascularcomplications • Hematologiccomplications • Neurologiccomplications • Bone ,phosphate & calcium abnormalities • Endocrinedisorders

  13. Hematologiccomplications in CRF • Normochromic normocytic anemia •  biosynthesis of erythropoetin • Bone-marrow depressive effect of uremic toxins • Hemolysis • GI loss of blood • Abnormal hemostasis •  bleeding time • Abnormal platelet aggregation &adhesiveness •  activity of platelet factor 3 • Enhanced susceptibility to infection

  14. Neurologic complications Uremic encephalopathy • Inability to concentrate, drowsiness • Insomnia, behavioral changes • Neuromuscular irritability • Hiccups, cramps, fasciculations • Asterixis, chorea, stupor, seizures Peripheral neuropathy Restless Legs

  15. Bone phosphate & calcium abnormalities in CRF •  biosynthesis of 1,25-dihidroksikolekalsiferol • Hypocalcemia • Hyperphosphatemia • Hyperparathyroidism • Acidosis • Renal • Osteodystrophy • Osteomalacia

  16. Endocrinedisorders in CRF • Secondary hyperparathyroidism • Glucose intolerance • Disturbances of insulin metabolism • Hyperinsulinemia • Peripheral insulin resitance • Pituitary, throid & adrenal are normal • Libido and fertility 

  17. Essentials of Diagnosis • Decline in the GFR over months to years. • Persistent proteinuria or abnormal renal morphology may be present. • Hypertension in most cases. • Symptoms and signs of uremia when nearing end-stage disease. • Bilateral small or echogenic kidneys on ultrasound in advanced disease.

  18. TREATMENT SlowingProgression • Treatment of the underlying cause of CKD is vital. Control of diabetes should be aggressive in early CKD; risk of hypoglycemia increases in advanced CKD, and glycemic targets may need to be relaxed to avoid this dangerous complication. • Blood pressure control is vital to slow progression of all forms of CKD; agents that block the renin-angiotensin-aldosterone system are particularly important in proteinuric disease • Current guidelines suggest a blood pressure goal of 130/80 mm Hg for patients with CKD; a goal of 125/75 mm Hg is recommended for patients with proteinuria.

  19. Dietary Management • Every patient with CKD should be evaluated by a renal nutritionist. Specific recommendations should be made concerning protein, salt, water, potassium, and phosphorus intake to help manage CKD progression and complications. • Protein restriction to 0.6–0.8 g/kg/d may retard CKD progression • Salt and water restriction. A goal of 2 g/d of sodium is reasonable for most patients. A daily intake of 2 L of fluid maintains water balance. • Potassium restriction. Restriction is needed once the GFR has fallen below 10–20 mL/min/1.73 m2, or earlier if the patient is hyperkalemic. Patients should receive detailed lists describing potassium content of foods and should limit their intake to < 50–60 mEq/d (2 g). • Phosphorus restriction. The phosphorus level should be kept in the ‘normal’ range (<4.5 mg/dL) predialysis,

  20. Medication Management • Many drugs are excreted by the kidney; dosages should be adjusted for GFR. • Insulin doses may need to be adjusted. • Magnesium-containing medications, such as laxatives or antacids, should be avoided as should phosphorus-containing medicines, particularly cathartics. • Morphine metabolites are active and can accrue in advanced CKD; • Drugs with potential nephrotoxicity (NSAIDs, intravenous contrast) should be avoided • The anemia of CKD is primarily due to decreased erythropoietin production, which often becomes clinically significant during stage 3 CKD. Many patients are iron deficient as well due to impaired GI iron absorption.

  21. Treatment of End-Stage Renal Disease HEMODIALYSIS END STAGE RENAL FAILURE TRANSPLANTATION PERITONEAL DIALYSIS When GFR declines to 5–10 mL/min/1.73 m2 (with or without overt uremic symptoms), renal replacement therapy (hemodialysis, peritoneal dialysis, or kidney transplantation) is required to sustain life.

  22. Kidney transplant sources • Living Related Unrelated • Deceased Xenotransplant ???

  23. Vascularaccessfor HD

  24. Native AV Fistula

  25. Vascular access for HD

  26. Principle of hemodialysis cellophane sausage casings, a cooling system from an old Ford, parts from a crashed German fighter plane, and washing machine tubs.

  27. Principle of PD

  28. When to Refer • Patient education is important in understanding which mode of therapy is most suitable, as is timely preparation for treatment; therefore, referral to a nephrologist should take place in late stage 3 CKD, or when the GFR is declining rapidly. Such referral has been shown to improve mortality • A patient with other forms of CKD such as those with significant proteinuria (> 1 g/d) or polycystic kidney disease should be referred to a nephrologist at earlier stages.

  29. Prognosis in ESRD • Compared with kidney transplant recipients and age-matched controls, mortality is higher for patients undergoing dialysis. There is likely little difference in survival for well-matched peritoneal versus hemodialysis patients. • Survival rates on dialysis depend on the underlying disease process. Five-year Kaplan-Meier survival rates vary from 36% for patients with diabetes to 53% for patients with glomerulonephritis. Overall 5-year survival is currently estimated at 39%. Patients undergoing dialysis have an average life-expectancy of 3–5 years, but survival for as long as 25 years may be achieved depending on comorbidities. • The most common cause of death is cardiac disease (50%). Other causes include infection, cerebrovascular disease, and malignancy.

  30. Case 1 • 35 years old male • Nocturia since 2006 • He had a history of pyelonephritis with kidney stones • Since then he had no hospital admission

  31. PHYSICAL EXAMINATION • BP: 186/100mmHg P: 90/min/R • Weight 72 kg, Height 175 cm • Temperature: 36.4 0C • Raised JVP • Dyspneic with crackles over the lung bases

  32. Laboratorytests • Hb: 10.6g/dl Htc:31.9% Na: 137mEq/L • Serum BUN: 78mg/dl ;Kr: 3.6mg/dL • Urinespecificgravity: 1012 • Ca  8.3mg/dL     Pi 4.6 mg/dLAlbumin 3.6 g/dLFe 16  ug/dL     (59 - 158 )          TIBC 205 ug/dL     (228 - 428)    

  33. What is yourlikely Diagnosis ?

  34. Estimated CrCl (Cockcroft-Gault formula) 140-age)x Wt 72 x pCr ForFemale= x0.85

  35. http://www.kidney.org/professionals/kdoqi/gfr_calculator.cfm

  36. Stage 4 CKD

  37. What else do you need to know?

  38. URINARY USG • RK 85 mm, 5x7 mm midpolekidneystone • LK 88 mm, 7x6 mm apicalpolekidneystone • GII RenalParenchimalDis. Proteinuria: 354 mg/day

  39. Renalbx. ? • Urinary CT? • UrinaryCa? • Stone analysis?

  40. How would you manage this patient?

  41. TreatmentStrategies • Anemia EPO, Parenterallyforms of iron • Hyperphosphatemia Phosphatebinders • HT Do not useACEIs+ARBs • Do not usecontrastagents • Do not useNSAIDs

  42. Case 2 • 48 yearsoldfemale • Leftflankpain, vomiting, fever • History of PCKD ( diagnosed in 1999) • Her motherdiedbecause of intracranialhemorage (AVM? and AVA?)

  43. PHYSICAL EXAMINATION • BP: 100/60mmHg P: 118/min/R • Weight 59 kg, 38.2 0C • Dyspne(+), tachipne (+) • turgor , Paleface, • Looksweakandunwell • fullness of neckveins (+)

  44. Laboratory tests • WBC: 12.860/mm3 • Hb: 12.2g/dl Htc:37.3% Na: 137mEq/L • BUN: 156mg/dl ;Kr: 10.3mg/dL • ABG analysis PH 7.26 • HCO3 12.8 BE-12 • Urinespecificgravity: 1010 • S.Na 133mEq/l S.K 6.7mEq/l • Ca  8.3mg/dL     Pi 6.8 mg/dL • CRP 184

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