Prof.Dr.P.Vijayaragavan. Dr.A.Vijayalakshmi. M4 Unit .
Kidney damage for more than 3 months as defined by functional and structural abnormalities of kidney with or without decreased GFR, that can lead to decreased GFR manifest by either  1.Pathological abnormality 2.Markers of kidney damage, including abnormality in the composition of blood or urine and imaging. 3.GFR <60ml/min for >3 months with or without kidney damage .
Chronic renal failure is the process of continuing significant irreversible reduction in nephron number. Classification   stage  GFR, ml/min per 1.73m*2 o  >90 1  >90 2  60-89 3  30-59 4  15-29 5  <15
1.Equation from the modification of Diet in Renal Disease  study Estimated GFR(ml/min per 1.73m*2)=1.86x(Pcr)*-1.154 X(age)*-0.203 Multiply by o.742 for women. 2.Cockcroft-Gault equation (140-agexbody weight in Kg)/72xPcr(mg/dl) multiply by 0.85 for women.
Nonmodifiable risk factors Age - The normal annual mean decline in GFR with age from the peak GFR12o ml/min, attained during the 3 rd  decade of life is 1ml/min per  year. And reaching GFR of 70ml at 70 years. Gender Male gender  is associated with rapid decline in GFR. Race Africans ,Americans have increased incidence of CKD. And U.K, Indo-Asian Diabetics have faster rate progression of CKD.
Modifiable risk factors Diabetes Hypertension Obesity Dyslipedimia Smoking Alcohol Caffeine Drugs;NSAID
1.Most frequent cause of CKD is Diabetic Nephropathy.(often type 2 DM). 2.Hypertensive nephropathy common cause in elderly. 3.Obesity has linked with IgA nephropathy . 4.Chronic glomerular nephritis . 5.Chronic interstitial nephritis. 6.Hereditary kidney diseases.
The primary damage can be glomerular,  vascular, interstitial, tubular  or  combination The kidney disease causes nephron destruction and loss of nephrons. Metabolic dysfunction , heavy  proteinuria,  systemic hypertension.
Initiating mechanisms specific to the underlying etiology. Progressive mechanisms, involving hyperfilteration and hypertrophy of the remaining viable nephrons,leading to increased pressure and flow predispose to sclerosis and drop out of the remaining nephrons .
Fluid and electrolyte disturbances Volume expansion Hyponatremia. Hyperkalemia. Hyperphosphatemia . Endocrine metabolic  Secondary hyperparathyroidism. Vit-D deficient  osteomalacia. Hyperuricemia. Hypertriglyceridemia .
Infertility and sexual dysfunction . Neuromuscular Fatigue Sleep disorders. Headache. Impaired mentation Lethargy. Asterixis. Peripheral neuropathy
Cardiovascular Hypertension CCF Pulmonary edema Pericarditis Cardiomyopathy Dermatology Hyperpigmentation Pruritis Echymosis .
GIT Anorexia Nausea, vomiting Peritonitis  GI bleed. Idiopathic ascites . Hematology Anemia Lymphocytopenia Thrombocytopenia, Leucopenia.
Between 50% t0 75% of individual with CKD stage 3 and 4 have H.T. Patients with stage 3 CKD have dyslipidemia. Anemia is associated with stage 3 CKD. The causes are 1.relative deficiency of erythropoietin 2.diminished RBC survival  3.bleeding diathesis  4.iron deficiency 5.chronic inflammation.  6.folate or vit B12 deficiency.
Elevation of growth hormones, Decrease T4,IncreaseT3 ,Decrease clearance of insulin. Elevated prolactin in males.Alteration in pituitary ovarian axis in females   are to be noted .
1.Dehydration. 2.Drugs. 3.Disease relapse. 4.Disease Acceleration 5.Infection. 6.Obstruction. 7.Hypercalcemia. 8.Hypertension. 9.Heart failure. 10.Interstitial nephritis .
1.Pericarditis. 2.Fluid overload.-Pulmonary edema. 3.Resistant Hypertension. 4.Hyperkalemia. 5.Uncompensated metabolic acidosis. 6.Seizures.
Glucose High in DM. Electrolytes Na-usually normal or low.,K+ raised.,HCO3 decreased. Serum Albumin-Hypoalbuminemia. Serum Ca+ may be normal or high. Phosphate high . Urea-When blood urea high  when compared to creatinine  evidence of dehydration, GIT blood loss,  infection should be thought. Serum creatinine  SAP - raised when bone disease develops . Serum PTH  raised .
Serum cholesteral  evidence of dyslipidemia . Hematology - Normocytic normochromic anemia . Serology AutoAb,Antinuclear Ab, AntiGBM Ab, Hepatitis B, HIV . Urine analysis RBC-Sediments GBN.,Pyuria-Interstitial nephritis. Spot urine collection for Total protein,creatinine ratio. Normal-is <2 24 urine forTotal protein and creatinine clearance. Serum and urine protein electrophoresis . ECG,ECHO - LVH .
Image Xray Nephrocalcinosis. U.S.G Small kidneys with reduced cortical thickness, showing increased echogenecity, scarring and multiple cysts suggests chronic process(large kidney-DM initial stage, Amyloidosis, HIV, Polycystic kidney disease.) CT ,MRI are helpful in Renal artery stenosis and renal vein thrombosis. Renal biopsy .
Measure  proteinuria  which is the strongest single predictor of GFR decline. Therapy induced proteinuria reduction ,slows GFR. Each 1gm reduction in protenuria by 4 to 6 months of the antiprotenuric  treatment, GFR decline is slowed by about 1 to 2 ml/min./yr. Measure GFR  ; Serial creatinine measurement is usually sufficient. Be aware the conditions can increase creatinine production 1.cooked meat, 2.fenofibrate therapy,  3.increased exercise 4.increased muscle mass. Decrease creatinine production  1.vegetarian diet, 2.muscle wasting , 3.decreased exercise .
Stage I and II  Usually asymptomatic patients. To modify the risk factors.SRD, Protein restricted diet, Stage3  :  creatinine  level  2mg/dl  H.T, secondary  Hyperparathyroidism To start phosphate restriction, phosphate binders,  treat H.T, immunize against  hepatitis B. Stage4   with serum creatinine level  4mg/dl  +anemia  To restrict dietry potassium to 60mmol/day. Add Erythropoietin  Advice moderate protein restriction and plan renal  replacement therapy including vascular access .
Stage5   serum creatinine level  8mg/dl ,  +sodium and  water retention, anorexia, vomiting, reduced higher mental functions. To plan elective start of dialysis or pre-emptive renal transplantation. Stage5 uremic emergency 17mg/dl  +pulmonary edema, fits, coma, metabolic acidosis, hyperkalemia, death To start dialysis or provide palliative care . .
When to refer the patient to Nephrologists Ideally  when the patients reach  CKD stage 3. Be aware that an arteriovenous fistula typically takes 8 to 12 weeks to mature . Prevent  late presentation of patients to the nephrologists  to start dialysis using central venous catheter s.
Hello Kidney _ YOU Are a KID KID NEE We will take care of you by modifying the risk factors, And by retarding the progression ,,,,,,. Physicians.
THANK YOU THANK YOU THANK YOU

CME: Chronic Renal failure

  • 1.
  • 2.
    Kidney damage formore than 3 months as defined by functional and structural abnormalities of kidney with or without decreased GFR, that can lead to decreased GFR manifest by either 1.Pathological abnormality 2.Markers of kidney damage, including abnormality in the composition of blood or urine and imaging. 3.GFR <60ml/min for >3 months with or without kidney damage .
  • 3.
    Chronic renal failureis the process of continuing significant irreversible reduction in nephron number. Classification stage GFR, ml/min per 1.73m*2 o >90 1 >90 2 60-89 3 30-59 4 15-29 5 <15
  • 4.
    1.Equation from themodification of Diet in Renal Disease study Estimated GFR(ml/min per 1.73m*2)=1.86x(Pcr)*-1.154 X(age)*-0.203 Multiply by o.742 for women. 2.Cockcroft-Gault equation (140-agexbody weight in Kg)/72xPcr(mg/dl) multiply by 0.85 for women.
  • 5.
    Nonmodifiable risk factorsAge - The normal annual mean decline in GFR with age from the peak GFR12o ml/min, attained during the 3 rd decade of life is 1ml/min per year. And reaching GFR of 70ml at 70 years. Gender Male gender is associated with rapid decline in GFR. Race Africans ,Americans have increased incidence of CKD. And U.K, Indo-Asian Diabetics have faster rate progression of CKD.
  • 6.
    Modifiable risk factorsDiabetes Hypertension Obesity Dyslipedimia Smoking Alcohol Caffeine Drugs;NSAID
  • 7.
    1.Most frequent causeof CKD is Diabetic Nephropathy.(often type 2 DM). 2.Hypertensive nephropathy common cause in elderly. 3.Obesity has linked with IgA nephropathy . 4.Chronic glomerular nephritis . 5.Chronic interstitial nephritis. 6.Hereditary kidney diseases.
  • 8.
    The primary damagecan be glomerular, vascular, interstitial, tubular or combination The kidney disease causes nephron destruction and loss of nephrons. Metabolic dysfunction , heavy proteinuria, systemic hypertension.
  • 9.
    Initiating mechanisms specificto the underlying etiology. Progressive mechanisms, involving hyperfilteration and hypertrophy of the remaining viable nephrons,leading to increased pressure and flow predispose to sclerosis and drop out of the remaining nephrons .
  • 10.
    Fluid and electrolytedisturbances Volume expansion Hyponatremia. Hyperkalemia. Hyperphosphatemia . Endocrine metabolic Secondary hyperparathyroidism. Vit-D deficient osteomalacia. Hyperuricemia. Hypertriglyceridemia .
  • 11.
    Infertility and sexualdysfunction . Neuromuscular Fatigue Sleep disorders. Headache. Impaired mentation Lethargy. Asterixis. Peripheral neuropathy
  • 12.
    Cardiovascular Hypertension CCFPulmonary edema Pericarditis Cardiomyopathy Dermatology Hyperpigmentation Pruritis Echymosis .
  • 13.
    GIT Anorexia Nausea,vomiting Peritonitis GI bleed. Idiopathic ascites . Hematology Anemia Lymphocytopenia Thrombocytopenia, Leucopenia.
  • 14.
    Between 50% t075% of individual with CKD stage 3 and 4 have H.T. Patients with stage 3 CKD have dyslipidemia. Anemia is associated with stage 3 CKD. The causes are 1.relative deficiency of erythropoietin 2.diminished RBC survival 3.bleeding diathesis 4.iron deficiency 5.chronic inflammation. 6.folate or vit B12 deficiency.
  • 15.
    Elevation of growthhormones, Decrease T4,IncreaseT3 ,Decrease clearance of insulin. Elevated prolactin in males.Alteration in pituitary ovarian axis in females are to be noted .
  • 16.
    1.Dehydration. 2.Drugs. 3.Diseaserelapse. 4.Disease Acceleration 5.Infection. 6.Obstruction. 7.Hypercalcemia. 8.Hypertension. 9.Heart failure. 10.Interstitial nephritis .
  • 17.
    1.Pericarditis. 2.Fluid overload.-Pulmonaryedema. 3.Resistant Hypertension. 4.Hyperkalemia. 5.Uncompensated metabolic acidosis. 6.Seizures.
  • 18.
    Glucose High inDM. Electrolytes Na-usually normal or low.,K+ raised.,HCO3 decreased. Serum Albumin-Hypoalbuminemia. Serum Ca+ may be normal or high. Phosphate high . Urea-When blood urea high when compared to creatinine evidence of dehydration, GIT blood loss, infection should be thought. Serum creatinine SAP - raised when bone disease develops . Serum PTH raised .
  • 19.
    Serum cholesteral evidence of dyslipidemia . Hematology - Normocytic normochromic anemia . Serology AutoAb,Antinuclear Ab, AntiGBM Ab, Hepatitis B, HIV . Urine analysis RBC-Sediments GBN.,Pyuria-Interstitial nephritis. Spot urine collection for Total protein,creatinine ratio. Normal-is <2 24 urine forTotal protein and creatinine clearance. Serum and urine protein electrophoresis . ECG,ECHO - LVH .
  • 20.
    Image Xray Nephrocalcinosis.U.S.G Small kidneys with reduced cortical thickness, showing increased echogenecity, scarring and multiple cysts suggests chronic process(large kidney-DM initial stage, Amyloidosis, HIV, Polycystic kidney disease.) CT ,MRI are helpful in Renal artery stenosis and renal vein thrombosis. Renal biopsy .
  • 21.
    Measure proteinuria which is the strongest single predictor of GFR decline. Therapy induced proteinuria reduction ,slows GFR. Each 1gm reduction in protenuria by 4 to 6 months of the antiprotenuric treatment, GFR decline is slowed by about 1 to 2 ml/min./yr. Measure GFR ; Serial creatinine measurement is usually sufficient. Be aware the conditions can increase creatinine production 1.cooked meat, 2.fenofibrate therapy, 3.increased exercise 4.increased muscle mass. Decrease creatinine production 1.vegetarian diet, 2.muscle wasting , 3.decreased exercise .
  • 22.
    Stage I andII Usually asymptomatic patients. To modify the risk factors.SRD, Protein restricted diet, Stage3 : creatinine level 2mg/dl H.T, secondary Hyperparathyroidism To start phosphate restriction, phosphate binders, treat H.T, immunize against hepatitis B. Stage4 with serum creatinine level 4mg/dl +anemia To restrict dietry potassium to 60mmol/day. Add Erythropoietin Advice moderate protein restriction and plan renal replacement therapy including vascular access .
  • 23.
    Stage5 serum creatinine level 8mg/dl , +sodium and water retention, anorexia, vomiting, reduced higher mental functions. To plan elective start of dialysis or pre-emptive renal transplantation. Stage5 uremic emergency 17mg/dl +pulmonary edema, fits, coma, metabolic acidosis, hyperkalemia, death To start dialysis or provide palliative care . .
  • 24.
    When to referthe patient to Nephrologists Ideally when the patients reach CKD stage 3. Be aware that an arteriovenous fistula typically takes 8 to 12 weeks to mature . Prevent late presentation of patients to the nephrologists to start dialysis using central venous catheter s.
  • 25.
    Hello Kidney _YOU Are a KID KID NEE We will take care of you by modifying the risk factors, And by retarding the progression ,,,,,,. Physicians.
  • 26.
    THANK YOU THANKYOU THANK YOU