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Chronic Kidney Disease, CKD, Nephrology,

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Chronic Kidney Disease, CKD, Nephrology, Specialty rounds, Internal Medicine, Uremia, CDUH, Evardone

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Chronic Kidney Disease, CKD, Nephrology,

  1. 1. Jose Socrates “Dee” Matuod Evardone Year Level 2 Nephrology 2 Chronic Kidney Disease • NEPHROLOGY ROUNDS
  2. 2. PRE TEST
  3. 3. PRETEST 1) Urine albumin per gram of creatinine content that signifies Chronic Renal Damage: A.17mg in males, 25mg in females B.25mg in males, 17mg in females C. 25mg in both sexes D. None of the above
  4. 4. PRETEST 2) In CKD with Uremia, these compounds with a molecular mass between 500 and 1500 Da, are also retained and contribute to morbidity and mortality A.Guanidino compounds B. products of nucleic acid metabolism C.Polyamines D.middle molecules
  5. 5. PRETEST 3) Diuretics used in combination of loop diuretics, which inhibits the sodium chloride co-transporter in the distal convoluted tubule, can help effect renal salt excretion: A. Ethacrynic acid B. Metolazone C. Acetazolamide D. Eplerenone
  6. 6. PRETEST 4) The combination of ACE inhibitor and ARB is associated with a greater reduction in proteinuria compared to either agent alone. True or False
  7. 7. PRETEST 5) Testing for microalbumin is recommended in all diabetic patients at least: A. Every 6 months B. Every 3 months C.Every 12 months D. Every clinic visit
  8. 8. PRETEST 6) CKD is defined by the presence of kidney damage or decreased kidney function, irrespective of the cause, for at least: A.2 months B.3 months C.6 months D. 12 months
  9. 9. PRETEST 7) In CKD dietary recommendation, at least how much of the protein intake should be of high biologic value: A.50% B. 40% C.60% D. 30%
  10. 10. PRETEST 8) In CKD, NO dose adjustment is needed for agents/drugs that are excreted by a nonrenal route by more than: A.50% B. 60% C.70% D. 80%
  11. 11. PRETEST 9) In CKD, educational programs should be commenced no later than stage __ CKD so that the patient has sufficient time and cognitive function to learn the important concepts, to make informed choices, and implement preparatory measures for renal replacement therapy. A.Stage 2 B. Stage 3 C.Stage 4 D. Stage 5
  12. 12. PRETEST 10) Parathyroid hormone(PTH) itself is considered a uremic toxin. True or False
  13. 13. Topic Outline • I INTRODUCTION • II CLINICAL AND LABORATORY MANIFESTATIONS OF CHRONIC KIDNEY DISEASE AND UREMIA • III EVALUATION AND MANAGEMENT OF PATIENTS WITH CKD • IV TREATMENT
  14. 14. Topic Outline I INTRODUCTION A. PATHOPHYSIOLOGY OF CHRONIC KIDNEY DISEASE B. IDENTIFICATION OF RISK FACTORS AND STAGING OF CKD C. ETIOLOGY AND EPIDEMIOLOGY D. PATHOPHYSIOLOGY AND BIOCHEMISTRY OF UREMIA
  15. 15. Topic Outline II CLINICAL AND LABORATORY MANIFESTATIONS OF CHRONIC KIDNEY DISEASE AND UREMIA A. FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS 1. Sodium and water homeostasis 2. Potassium homeostasis 3. Metabolic acidosis B. DISORDERS OF CALCIUM AND PHOSPHATE METABOLISM 1. Bone manifestations of CKD 2. Calcium, phosphorus, and the cardiovascular system 3. Other complications of abnormal mineral metabolism C. CARDIOVASCULAR ABNORMALITIES 1. Ischemic vascular disease 2. Heart failure 3. Hypertension and left ventricular hypertrophy 4. Pericardial disease
  16. 16. Topic Outline II CLINICAL AND LABORATORY MANIFESTATIONS OF CHRONIC KIDNEY DISEASE AND UREMIA D. HEMATOLOGIC ABNORMALITIES 1. Anemia 2. Abnormal hemostasis E. NEUROMUSCULAR ABNORMALITIES F. GASTROINTESTINAL AND NUTRITIONAL ABNORMALITIES G. ENDOCRINE-METABOLIC DISTURBANCES H. DERMATOLOGIC ABNORMALITIES
  17. 17. Topic Outline III EVALUATION AND MANAGEMENT OF PATIENTS WITH CKD A.INITIAL APPROACH 1.History and physical examination 2.Laboratory investigation 3.Imaging studies 4.Renal biopsy B.ESTABLISHING THE DIAGNOSIS AND ETIOLOGY OF CKD
  18. 18. Topic Outline IV TREATMENT A. SLOWING THE PROGRESSION OF CKD 1. Reducing Intraglomerular Hypertension and Proteinuria B. SLOWING PROGRESSION OF DIABETIC RENAL DISEASE 1. Control of Blood Glucose 2. Control of Blood Pressure and Proteinuria 3. Protein Restriction C. MANAGING OTHER COMPLICATIONS OF CHRONIC KIDNEY DISEASE 1. Medication Dose Adjustment 2. Preparation for Renal Replacement Therapy 3. Patient Education
  19. 19. CASE E.R. 63M HTN>10yrs, poor med compliance nonDM previously smoker(stopped 15ys ago) alcoholic beverage drinker(2beer/week) CC: DYSPNEA
  20. 20. CASE HPI: 1 month ago: exertional dyspnea plus, 2 pillow orthopnea, loss of appetite, body malaise, nausea and vomiting admitted at CVGH, creatinine was 20mg/dl, px was advised for hemodialysis (did not consent)
  21. 21. CASE HPI: 1 week PTA: Bilateral LE swelling weight loss Oliguria Dyspnea at rest
  22. 22. Awake, in respiratory distress Anicteric sclerae, Pale palpebral conjunctivae C/L: Equal chest expansion, bibasal rales, decrease breath soundson the left lower lobe CVS: Distinct heart sounds, normal rate, regular rhythm ABD: Normoactive bowel sounds, soft, non tender, no organomegaly NEURO: Unremarkable BP: 190/100mmHg PR: 98 bpm RR: 35 cpm Temp: 36.2°C P.E. SKIN: cold,clammy EXT: Bipedal edema grade 3
  23. 23. ECG
  24. 24. LABS RENAL PANEL C CBC Adm Hgb 5.4 Hct 16.8 WBC Seg Bas Eos Lymph Mono 11.3 95 0 0 2 3 RBC 2.56 Platelet 121 MCV MCH MCHC 65.6 21.1 32.2 ABG pH 6.99 pCO2 17 pO2 300 HCO3 4.2 fiO2 60% SO2 100% pF ratio 500 Temp 36.2
  25. 25. LABS RENAL PANEL C Glucose 107 mg/dl BUN 197 mg/dl Creatinine 37.8 mg/dl Uric Acid 8.7 mg/dl Calcium 5.6 mg/dl Phosphorus 17.6 mg/dl Sodium 127 mmol/L Potassium 6.8 mmol/L Chloride 89 mmol/L Enz. CO2 8.0 mmol/L Total Chole 99 mg/dl Triglycerides 103 mg/dl Total Protein 5.4 g/dL Albumin 2.9 g/dL Globulin 2.5 g/dL A/G Ratio 0.7 SGPT/ALT 38 U/L Allk Phos 70 U/
  26. 26. IMPRESSION 1. ESRD with Uremia sec. to Hypertensive Nephrosclerosis 2. Pulmonary Congestion sec . to Fluid Overload sec. to #1 3. Metabolic acidosis, part. Compensated sec. to #1 4. Electrolyte Imbalance sec to #1 5. Essential Hypertension 6. CAP-High Risk 7. Microcytic, Hypochromic Anemia sec to #1
  27. 27. Abbreviations • NKF - National Kidney Foundation • KDOQI - Kidney Disease Outcomes Quality Initiative • KDIGO - Kidney Disease Improving Global Outcomes
  28. 28. What is CKD? • CKD is defined by the – presence of kidney damage or decreased kidney function – for three or more months, – irrespective of the cause.
  29. 29. What is CKD? • The persistence of the damage or decreased function for at least three months is necessary to distinguish CKD from acute kidney disease. • Kidney damage refers to pathologic abnormalities, whether established via: 1. renal biopsy or 2. imaging studies, or 3. inferred from markers such as a) urinary sediment abnormalities or b) increased rates of urinary albumin excretion.
  30. 30. What is CKD? • Chronic kidney disease is defined based on the presence of either kidney damage or decreased kidney function for three or more months, irrespective of cause. • Criteria: Duration ≥3 months, based on documentation or inference Glomerular filtration rate (GFR) <60 mL/min/1.73 m2 Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
  31. 31. CHRONIC KIDNEY DISEASE Duration ≥3 months, based on documentation or inference Duration is necessary to distinguish chronic from acute kidney diseases. 1. Clinical evaluation can often suggest duration 2. Documentation of duration is usually not available in epidemiologic studies
  32. 32. CHRONIC KIDNEY DISEASE GFR is the best overall index of kidney function in health and disease. 1. The normal GFR in young adults is approximately 125 mL/min/1.73 m2; GFR <15 mL/min/1.73 m2 is defined as kidney failure 2. Decreased GFR can be detected by current estimating equations for GFR based on serum creatinine (estimated GFR) but not by serum creatinine alone 3. Decreased estimated GFR can be confirmed by measured GFR Glomerular filtration rate (GFR) <60 mL/min/1.73 m2
  33. 33. CHRONIC KIDNEY DISEASE A) Pathologic abnormalities (examples). Cause is based on underlying illness and pathology. Markers of kidney damage may reflect pathology. 1. Glomerular diseases (diabetes, autoimmune diseases, systemic infections, drugs, neoplasia) 2. Vascular diseases (atherosclerosis, hypertension, ischemia, vasculitis, thrombotic microangiopathy) 3. Tubulointerstitial diseases (urinary tract infections, stones, obstruction, drug toxicity) 4. Cystic disease (polycystic kidney disease) Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
  34. 34. CHRONIC KIDNEY DISEASE B) History of kidney transplantation. In addition to pathologic abnormalities observed in native kidneys, common pathologic abnormalities include the following: 1. Chronic allograft nephropathy (non-specific findings of tubular atrophy, interstitial fibrosis, vascular and glomerular sclerosis) 2. Rejection 3. Drug toxicity (calcineurin inhibitors) 4. BK virus nephropathy 5. Recurrent disease (glomerular disease, oxalosis, Fabry disease) Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
  35. 35. CHRONIC KIDNEY DISEASE C) Albuminuria as a marker of kidney damage (increased glomerular permeability, urine albumin-to-creatinine ratio [ACR] >30 mg/g).* 1. The normal urine ACR in young adults is <10 mg/g. Urine ACR categories 10-29, 30-300 and >300 mg are termed "high normal, high, and very high" respectively. Urine ACR >2200 mg/g is accompanied by signs and symptoms of nephrotic syndrome 2. Threshold value corresponds approximately to urine dipstick values of trace or 1+ 3. High urine ACR can be confirmed by urine albumin excretion in a timed urine collection Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
  36. 36. CHRONIC KIDNEY DISEASE D) Urinary sediment abnormalities as markers of kidney damage 1. RBC casts in proliferative glomerulonephritis 2. WBC casts in pyelonephritis or interstitial nephritis 3. Oval fat bodies or fatty casts in diseases with proteinuria 4. Granular casts and renal tubular epithelial cells in many parenchymal diseases (non-specific) Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
  37. 37. CHRONIC KIDNEY DISEASE E) Imaging abnormalities as markers of kidney damage (ultrasound, computed tomography and magnetic resonance imaging with or without contrast, isotope scans, angiography). 1. Polycystic kidneys 2. Hydronephrosis due to obstruction 3. Cortical scarring due to infarcts, pyelonephritis or vesicoureteral reflux 4. Renal masses or enlarged kidneys due to infiltrative diseases 5. Renal artery stenosis 6. Small and echogenic kidneys (common in later stages of CKD due to many parenchymal diseases) Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
  38. 38. PATHOPHYSIOLOGY OF CHRONIC KIDNEY DISEASE Two broad sets of mechanisms of damage: 1. initiating mechanisms specific to the underlying etiology 2. a set of progressive mechanisms - hyperfiltration and hypertrophy of the remaining viable nephrons
  39. 39. PATHOPHYSIOLOGY OF CHRONIC KIDNEY DISEASE Two broad sets of mechanisms of damage: 1. initiating mechanisms specific to the underlying etiology 2. a set of progressive mechanisms - hyperfiltration and hypertrophy of the remaining viable nephrons
  40. 40. PATHOPHYSIOLOGY OF CHRONIC KIDNEY DISEASE Increased intrarenal activity of the renin- angiotensin axis appears to contribute both to: initial adaptive hyperfiltration the subsequent maladaptive hypertrophy and sclerosis (TGF-β)
  41. 41. Left: Schema of the normal glomerular architecture. Right: Secondary glomerular changes
  42. 42. IDENTIFICATION OF RISK FACTORS AND STAGING OF CKD Risk factors: 1. hypertension, 2. diabetes mellitus, 3. autoimmune disease, 4. older age, 5. African ancestry, 6. a family history of renal disease, 7. a previous episode of acute kidney injury, 8. and the presence of a. proteinuria, b. abnormal urinary sediment, or c. structural abnormalities of the urinary tract
  43. 43. Recommended Equations for Estimation of Glomerular Filtration Rate (GFR) Using Serum Creatinine Concentration (PCr), Age, Sex, Race, and Body Weight 1) Equation from the Modification of Diet in Renal Disease study∗ (MDRD) 2) Cockcroft-Gault equation
  44. 44. CKD
  45. 45. IDENTIFICATION OF RISK FACTORS AND STAGING OF CKD Chronic renal damage Persistence in the urine of:  >17 mg of albumin per gram of creatinine in adult males and  25 mg albumin per gram of creatinine in adult females
  46. 46. ETIOLOGY AND EPIDEMIOLOGY Leading Categories of Etiologies of CKD∗  Diabetic glomerular disease  Glomerulonephritis  Hypertensive nephropathy  Primary glomerulopathy with hypertension  Vascular and ischemic renal disease  Autosomal dominant polycystic kidney disease  Other cystic and tubulointerstitial nephropathy
  47. 47. ETIOLOGY AND EPIDEMIOLOGY Newly diagnosed CKD: present with hypertension CKD is often attributed to hypertension: When no overt evidence for a primary glomerular or tubulointerstitial kidney disease process is present
  48. 48. ETIOLOGY AND EPIDEMIOLOGY Two Categories: 1) patients with a silent primary glomerulopathy 2) patients in whom progressive nephrosclerosis and hypertension is the renal correlate of a systemic vascular disease
  49. 49. Multiple Functions of the Kidneys 1) Excretion of metabolic waste products and foreign chemicals 2) Regulation of water and electrolyte balances 3) Regulation of body fluid osmolality and electrolyte concentrations 4) Regulation of arterial pressure 5) Regulation of acid-base balance 6) Secretion, metabolism, and excretion of hormones 7) Gluconeogenesis
  50. 50. PATHOPHYSIOLOGY AND BIOCHEMISTRY OF UREMIA Elevated waste products: Hundreds of toxins, water-soluble, hydrophobic, protein- bound, charged, and uncharged compounds, guanidino compounds, urates and hippurates, products of nucleic acid metabolism, polyamines, myoinositol, phenols, benzoates, and indoles ‘middle molecules’
  51. 51. PATHOPHYSIOLOGY AND BIOCHEMISTRY OF UREMIA A host of metabolic and endocrine functions normally performed by the kidneys is also impaired or suppressed:  anemia,  malnutrition,  and abnormal metabolism of carbohydrates, fats, and proteins
  52. 52. PATHOPHYSIOLOGY AND BIOCHEMISTRY OF UREMIA Urinary retention, decreased degradation, or abnormal regulation of hormones PTH, FGF-23, insulin, glucagon, steroid hormones including vitamin D and sex hormones, and prolactin
  53. 53. 3 Spheres of dysfunction of Uremic Syndrome Toxins Homeostasis Progressive systemic inflammation UREM
  54. 54. CLINICAL AND LABORATORY MANIFESTATIONS OF CHRONIC KIDNEY DISEASE AND UREMIA
  55. 55. CLINICAL ABNORMALITIES IN UREMIA 1. Fluid and electrolyte disturbances 2. Endocrine-metabolic disturbances 3. Neuromuscular disturbances 4. Cardiovascular and pulmonary disturbances 5. Dermatologic disturbances 6. Gastrointestinal disturbances 7. Hematologic and immunologic disturbances (I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy.
  56. 56. CLINICAL ABNORMALITIES IN UREMIA 1. Fluid and electrolyte disturbances a. Volume expansion (I) b. Hyponatremia (I) c. Hyperkalemia (I) d. Hyperphosphatemia (I) (I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy.
  57. 57. CLINICAL ABNORMALITIES IN UREMIA 1. Secondary hyperparathyroidism (I or P) 2. Adynamic bone (D) 3. Vitamin D–deficient osteomalacia (I) 4. Carbohydrate resistance (I) 5. Hyperuricemia (I or P) 6. Hypertriglyceridemia (I or P) 7. Increased Lp(a) level (P) 8. Decreased high-density lipoprotein level (P) 9. Protein-energy malnutrition (I or P) 10.Impaired growth and development (P) 11.Infertility and sexual dysfunction (P) 12.Amenorrhea (I/P) 13.β2-Microglobulin– associated amyloidosis (P or D) (I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy. 2. Endocrine-metabolic disturbances
  58. 58. CLINICAL ABNORMALITIES IN UREMIA 1. Fatigue (I)b 2. Sleep disorders (P) 3. Headache (P) 4. Impaired mentation (I)b 5. Lethargy (I)b 6. Asterixis (I) 7. Muscular irritability 8. Peripheral neuropathy (I or P) 9. Restless legs syndrome (I or P) 10.Myoclonus (I) 11.Seizures (I or P) 12.Coma (I) 13.Muscle cramps (P or D) 14.Dialysis disequilibrium syndrome (D) 15.Myopathy (P or D) (I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy. 3. Neuromuscular disturbances
  59. 59. CLINICAL ABNORMALITIES IN UREMIA 1. Arterial hypertension (I or P) 2. Congestive heart failure or pulmonary edema (I) 3. Pericarditis (I) 4. Hypertrophic or dilated cardiomyopathy (I, P, or D) 5. Uremic lung (I) 6. Accelerated atherosclerosis (P or D) 7. Hypotension and arrhythmias (D) 8. Vascular calcification (P or D) (I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy. 4. Cardiovascular and pulmonary disturbances
  60. 60. CLINICAL ABNORMALITIES IN UREMIA 1.Pallor (I)b 2.Hyperpigmentation (I, P, or D) 3.Pruritus (P) 4.Ecchymoses (I) 5.Nephrogenic fibrosing dermopathy (D) 6.Uremic frost (I) (I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy. 5. Dermatologic disturbances
  61. 61. CLINICAL ABNORMALITIES IN UREMIA 1.Anorexia (I) 2.Nausea and vomiting (I) 3.Gastroenteritis (I) 4.Peptic ulcer (I or P) 5.Gastrointestinal bleeding (I, P, or D) 6.Idiopathic ascites (D) 7.Peritonitis (D) (I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy. 6. Gastrointestinal disturbances
  62. 62. CLINICAL ABNORMALITIES IN UREMIA 1.Anemia (I)b 2.Lymphocytopenia (P) 3.Bleeding diathesis (I or D)b 4.Increased susceptibility to infection 5.(I or P) 6.Leukopenia (D) 7.Thrombocytopenia (D) (I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy. 7. Hematologic and immunologic disturbances
  63. 63. FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS S O D I U M
  64. 64. FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS Hyponatremia – water restriction ECFV expansion – salt restriction Thiazides – limited utility in stages 3-5 CKD - loop diuretics needed Loop Diuretics resistance – Higher doses Metolazone – combined with loop diuretics, which inhibits the sodium chloride co-transporter of the distal convoluted tubule, can help effect renal salt excretion S O D I U M
  65. 65. FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS • HYPERKALEMIA • Precipitated by • increased dietary potassium intake, • protein catabolism, • hemolysis, • hemorrhage, • transfusion of stored red blood cells, • and metabolic acidosis • Medications P O T A S S I U M
  66. 66. RenalPotassiumHandling
  67. 67. FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS Hypokalemia: • Not common in CKD • reduced dietary potassium intake • GI losses • Diuretic therapy • Fanconi’s syndrome • RTA • Hereditary or acquired Tubulointerstitial disease P O T A S S I U M
  68. 68. FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS Metabolic acidosis • common disturbance in advanced CKD • combination of hyperkalemia and hyperchloremic metabolic acidosis is often present, even at earlier stages of CKD (stages 1–3) • Treat hyperkalemia • the pH is rarely <7.35 • usually be corrected with oral sodium bicarbonate supplementation M E T A C I D O S I S
  69. 69. FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS Renal Control of Acid-Base Balance 1) Secretion of H+ and Reabsorption of HCO3 by the Renal Tubules a. H+ is Secreted by Secondary Active Transport in the Early Tubular Segments b. Filtered HCO3 is Reabsorbed by Interaction with H+ in the Tubules c. Primary Active Secretion of H+ in the Intercalated Cells of Late Distal and Collecting Tubules 2) Combination of Excess H+ with Phosphate and Ammonia Buffers in the Tubule Generates “New” HCO3 a. Phosphate Buffer System Carries Excess H+ into the Urine and Generates New HCO3 b. Excretion of Excess H+ and Generation of New HCO3 by the Ammonia Buffer System M E T A C I D O S I S
  70. 70. RenalHandlingofAcid Excretion
  71. 71. • To maintain euvolemia: • Adjustments in the dietary intake of salt • and use of loop diuretics, occasionally in combination with metolazone • Hyponatremia: • water restriction • Hyperkalemia • responds to dietary restriction of potassium, • avoidance of potassium supplements • use of kaliuretic diuretics • potassium-binding resins, such as calcium resonium or sodium polystyrene • The renal tubular acidosis and subsequent anion- gap metabolic acidosis • alkali supplementation, typically with sodium bicarbonate
  72. 72. DISORDERS OF CALCIUM AND PHOSPHATE METABOLISM The principal complications of abnormalities of calcium and phosphate metabolism in CKD 1. occur in the skeleton and 2. the vascular bed, 3. with occasional severe involvement of extraosseous soft tissues Bone manifestations of CKD, classified as: • associated with high bone turnover with increased PTH levels • low bone turnover with low or normal PTH levels
  73. 73. DISORDERS OF CALCIUM AND PHOSPHATE METABOLISM The pathophysiology of secondary hyperparathyroidism: 1. Declining GFR leads to reduced excretion of phosphate 2. increased synthesis of PTH and growth of parathyroid gland mass 3. decreased levels of ionized calcium, resulting from diminished calcitriol production by the failing kidney Fibroblast growth factor 23 (FGF-23) (1) increased renal phosphate excretion; (2) stimulation of PTH, which also increases renal phosphate excretion; and (3) suppression of the formation of 1,25(OH)2D3, leading to diminished phosphorus absorption from the gastrointestinal tract
  74. 74. DISORDERS OF CALCIUM AND PHOSPHATE METABOLISM Osteitis fibrosa cystica  bone turnover  abnormal histology  brown tumor Low-turnover bone disease can be grouped into two categories: 1. adynamic bone disease 2. and osteomalacia
  75. 75. DISORDERS OF CALCIUM AND PHOSPHATE METABOLISM Calcium, phosphorus, and the cardiovascular system: • Hyperphosphatemia and hypercalcemia are associated with increased vascular calcification • calcification of the media in coronary arteries and even heart valves • ingested calcium cannot be deposited in bones with low turnover • osteoporosis and vascular calcification • hyperphosphatemia can induce a change in gene expression in vascular cells
  76. 76. DISORDERS OF CALCIUM AND PHOSPHATE METABOLISM Other complications of abnormal mineral metabolism: • Calciphylaxis (calcific uremic arteriolopathy) • Other etiologies • use of oral calcium as a phosphate binder • Warfarin
  77. 77. Sevelamer and lanthanum – non calcium containing polymers Calcitriol exerts a direct suppressive effect on PTH secretion and also indirectly suppresses PTH secretion by raising the concentration of ionized calcium recommended target PTH level between 150 and 300 pg/mL
  78. 78. CARDIOVASCULAR ABNORMALITIES 1) Ischemic vascular disease The CKD-related risk factors comprise 1. anemia, 2. hyperphosphatemia, 3. hyperparathyroidism, 4. sleep apnea, and 5. generalized inflammation Cardiac troponin levels are frequently elevated in CKD without evidence of acute ischemia.
  79. 79. CARDIOVASCULAR ABNORMALITIES 2) Heart failure “bat wing” distribution - form of “low- pressure” pulmonary edema
  80. 80. CARDIOVASCULAR ABNORMALITIES 3) Hypertension and left ventricular hypertrophy • anemia and the placement of an arteriovenous fistula • low blood pressure actually carries a worse prognosis than does high blood pressure • erythropoiesis-stimulating agents
  81. 81. MANAGEMENT OF HYPERTENSION • Blood pressure should be reduced to 125/75 • Salt restriction should be the first line of therapy MANAGEMENT OF CARDIOVASCULAR DISEASE • Lifestyle changes, including regular exercise • Manage dyslipidemia
  82. 82. Pericardial disease Chest pain with respiratory accentuation, accompanied by a friction rub, is diagnostic of pericarditis. Classic electrocardiographic abnormalities include PR-interval depression and diffuse ST-segment elevation Initiation of dialysis No heparin
  83. 83. HEMATOLOGIC ABNORMALITIES Anemia A normocytic, normochromic anemia is observed as early as stage 3 CKD and is almost universal by stage 4. The primary cause in patients with CKD is insufficient production of erythropoietin (EPO) by the diseased kidneys.
  84. 84. Causes of Anemia in CKD 1. Relative deficiency of erythropoietin 2. Diminished red blood cell survival 3. Bleeding diathesis 4. Iron deficiency 5. Hyperparathyroidism/bone marrow fibrosis 6. “Chronic inflammation” 7. Folate or vitamin B12 deficiency 8. Hemoglobinopathy 9. Comorbid conditions: hypo/hyperthyroidism, pregnancy, HIV-associated disease, autoimmune disease, immunosuppressive drugs
  85. 85. recombinant human EPO and modified EPO Products Use of EPO in CKD may be associated with an: 1. increased risk of stroke in those with type 2 diabetes, 2. an increase in thromboembolic events, 3. and perhaps a faster progression to the need for dialysis target a hemoglobin concentration of 100–115 g/L
  86. 86. HEMATOLOGIC ABNORMALITIES Abnormal hemostasis 1. prolonged bleeding time, 2. decreased activity of platelet factor III, 3. abnormal platelet aggregation and adhesiveness, 4. and impaired prothrombin consumption. Clinical manifestations include 1. an increased tendency to bleeding and bruising, 2. prolonged bleeding from surgical incisions, 3. menorrhagia, 4. and spontaneous GI bleeding
  87. 87. Abnormal bleeding time and coagulopathy in patients with renal failure may be reversed temporarily with • desmopressin(DDAVP), • cryoprecipitate, • IV conjugated estrogens, • blood transfusions, and • EPO therapy. Optimal dialysis will usually correct a prolonged bleeding time.
  88. 88. NEUROMUSCULAR ABNORMALITIES Central nervous system (CNS), peripheral, and autonomic neuropathy mild disturbances in memory and concentration and sleep disturbance. Neuromuscular irritability, including hiccups, cramps, and fasciculations or twitching of muscles, becomes evident at later stages. In advanced untreated kidney failure, asterixis, myoclonus, seizures, and coma can be seen
  89. 89. GASTROINTESTINAL AND NUTRITIONAL ABNORMALITIES Uremic fetor , a urine-like odor on the breath, derives from the breakdown of urea to ammonia in saliva and is often associated with an unpleasant metallic taste (dysgeusia)
  90. 90. DERMATOLOGIC ABNORMALITIES Pruritus nephrogenic fibrosing dermopathy
  91. 91. EVALUATION AND MANAGEMENT OF PATIENTS WITH CKD Laboratory investigation Serial measurements of renal function Serum concentrations of calcium, phosphorus, vitamin D, and PTH should be measured to evaluate metabolic bone disease. Hemoglobin concentration, iron, B 12 , and Folate A 24-h urine collection
  92. 92. EVALUATION AND MANAGEMENT OF PATIENTS WITH CKD Imaging studies most useful imaging study is a renal ultrasound CKD with normal sized kidneys DM nephropathy amyloidosis HIV nephropathy voiding cystogram judicious administration of sodium bicarbonate- containing solutions and N -acetyl-cysteine
  93. 93. ESTABLISHING THE DIAGNOSIS AND ETIOLOGY OF CKD Renal biopsy Contraindications: • bilaterally small kidneys • uncontrolled hypertension, • active urinary tract infection, • bleeding diathesis (including ongoing anticoagulation), • and severe obesity
  94. 94. EVALUATION AND MANAGEMENT OF PATIENTS WITH CKD The most important initial diagnostic step in the evaluation of a patient presenting with elevated serum creatinine is to distinguish newly diagnosed CKD from acute or subacute renal failure SUGGESTS CHRONICITY 1. hyperphosphatemia, 2. hypocalcemia, 3. elevated PTH and bone alkaline Phosphatase 4. Normochromic, normocytic anemia 5. bilaterally reduced kidney size <8.5 cm
  95. 95. Topic Outline IV TREATMENT A.SLOWING THE PROGRESSION OF CKD 1. Reducing Intraglomerular Hypertension and Proteinuria B. SLOWING PROGRESSION OF DIABETIC RENAL DISEASE 1. Control of Blood Glucose 2. Control of Blood Pressure and Proteinuria 3. Protein Restriction C.MANAGING OTHER COMPLICATIONS OF CHRONIC KIDNEY DISEASE 1. Medication Dose Adjustment 2. Preparation for Renal Replacement Therapy 3. Patient Education
  96. 96. TREATMENT
  97. 97. TREATMENT Any acceleration in the rate of decline should prompt a search for superimposed acute or subacute processes that may be reversible 1. ECFV depletion, 2. uncontrolled hypertension, 3. urinary tract infection, 4. new obstructive uropathy, 5. exposure to nephrotoxic agents 6. and reactivation or flare of the original 7. disease, such as lupus or vasculitis
  98. 98. TREATMENT SLOWING THE PROGRESSION OF CKD: Reducing Intraglomerular Hypertension and Proteinuria renoprotective effect of antihypertensive medications - ↓proteinuria 125/75 mmHg as the target blood pressure ACE inhibitors and ARBs Adverse effects from these agents include cough and angioedema with ACE inhibitors, anaphylaxis, and hyperkalemia with either class 2nd line - diltiazem and verapamil
  99. 99. TREATMENT SLOWING PROGRESSION OF DIABETIC RENAL DISEASE Control of Blood Glucose preprandial glucose be kept in the 5.0–7.2 mmol/L, (90–130 mg/dL) hemoglobin A 1C should be < 7% use and dose of oral hypoglycemic needs to be reevaluated Chlorpropramide Metformin Thiazolidinediones
  100. 100. TREATMENT SLOWING PROGRESSION OF DIABETIC RENAL DISEASE Control of Blood Pressure and Proteinuria albuminuria a strong predictor of cardiovascular events and nephropathy Microalbumin testing At least ANNUALLY
  101. 101. TREATMENT SLOWING PROGRESSION OF DIABETIC RENAL DISEASE Protein Restriction CKD – 0.60 and 0.75 g/kg per day at least 50% of the protein intake be of high biologic value Stage 5 CKD - 0.9g/kg/day Caloric requirement – 35cal/kg/day
  102. 102. TREATMENT MANAGING OTHER COMPLICATIONS OF CHRONIC KIDNEY DISEASE 1. Medication Dose Adjustment loading dose – no dose adjustment >70% excretion is by a nonrenal route – no adjustment NSAIDs should be avoided Nephrotoxic medical imaging radiocontrast agents and gadolinium should be avoided http://www.globalrph.com/renaldosing2.htm
  103. 103. TREATMENT MANAGING OTHER COMPLICATIONS OF CHRONIC KIDNEY DISEASE 1. Medication Dose Adjustment 2. Preparation for Renal Replacement Therapy symptoms and signs of impending uremia, such as anorexia, nausea, vomiting, lassitude – RX with Protein restriction optimal time for initiation of renal replacement therapy have been established – KDOQI Delaying – worse prognosis
  104. 104. HEMODIALYSIS ABSOLUTE INDICATIONS: ●Uremic pericarditis or pleuritis ●Uremic encephalopathy Common indications: 1. Declining nutritional status 2. Persistent or difficult to treat volume overload 3. Fatigue and malaise 4. Mild cognitive impairment 5. Refractory acidosis, hyperkalemia, and hyperphosphatemia
  105. 105. TREATMENT MANAGING OTHER COMPLICATIONS OF CHRONIC KIDNEY DISEASE 1. Medication Dose Adjustment 2. Preparation for Renal Replacement Therapy 3. Patient Education Kidney transplantation - offers the best potential for complete rehabilitation
  106. 106. THANK YOU
  107. 107. PRETEST 1) Urine albumin per gram of creatinine content that signifies Chronic Renal Damage: A.17mg in males, 25mg in females B.25mg in males, 17mg in females C. 25mg in both sexes D. None of the above
  108. 108. PRETEST 2) In CKD with Uremia, these compounds with a molecular mass between 500 and 1500 Da, are also retained and contribute to morbidity and mortality A.Guanidino compounds B. products of nucleic acid metabolism C.Polyamines D.middle molecules
  109. 109. PRETEST 3) Diuretics used in combination of loop diuretics, which inhibits the sodium chloride co-transporter in the distal convoluted tubule, can help effect renal salt excretion: A. Ethacrynic acid B. Metolazone C. Acetazolamide D. Eplerenone
  110. 110. PRETEST 4) The combination of ACE inhibitor and ARB is associated with a greater reduction in proteinuria compared to either agent alone. True or False
  111. 111. PRETEST 5) Testing for microalbumin is recommended in all diabetic patients at least: A. Every 6 months B. Every 3 months C.Every 12 months D. Every clinic visit
  112. 112. PRETEST 6) CKD is defined by the presence of kidney damage or decreased kidney function, irrespective of the cause, for at least: A.2 months B.3 months C.6 months D. 12 months
  113. 113. PRETEST 7) In CKD dietary recommendation, at least how much of the protein intake should be of high biologic value: A.50% B. 40% C.60% D. 30%
  114. 114. PRETEST 8) In CKD, NO dose adjustment is needed for agents/drugs that are excreted by a nonrenal route by more than: A.50% B. 60% C.70% D. 80%
  115. 115. PRETEST 9) In CKD, educational programs should be commenced no later than stage __ CKD so that the patient has sufficient time and cognitive function to learn the important concepts, to make informed choices, and implement preparatory measures for renal replacement therapy. A.Stage 2 B. Stage 3 C.Stage 4 D. Stage 5
  116. 116. PRETEST 10) Parathyroid hormone(PTH) itself is considered a uremic toxin. True or False
  117. 117. RenalPotassiumHandling
  118. 118. RenalCalciumandPhosphate Handling
  119. 119. Chronic Kidney Disease
  120. 120. Leading Categories of Etiologies of CKD∗
  121. 121. Chronic Kidney Disease NEPHROLOGY ROUNDS Jose Socrates M. Evardone Year Level 2 Nephrology 2
  122. 122. RenalPotassiumHandling
  123. 123. Normal Lab Values

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