CME: Chronic Renal failure
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CME: Chronic Renal failure

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CME: Chronic Renal failure CME: Chronic Renal failure Presentation Transcript

  • 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