CME: Chronic Renal failure

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 abnormality2.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 factorsAge- The normal annual mean decline in GFR with

age from the peak GFR12o ml/min, attained during the 3rd 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 factorsDiabetesHypertensionObesityDyslipedimiaSmokingAlcoholCaffeineDrugs;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 disturbancesVolume expansionHyponatremia.Hyperkalemia.Hyperphosphatemia.Endocrine metabolic Secondary hyperparathyroidism.Vit-D deficient osteomalacia.Hyperuricemia.Hypertriglyceridemia.

Infertility and sexual dysfunction.NeuromuscularFatigueSleep disorders.Headache.Impaired mentationLethargy.Asterixis.Peripheral neuropathy

CardiovascularHypertensionCCFPulmonary edemaPericarditisCardiomyopathyDermatologyHyperpigmentationPruritisEchymosis.

GITAnorexiaNausea, vomitingPeritonitis GI bleed.Idiopathic ascites.HematologyAnemiaLymphocytopeniaThrombocytopenia, 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 Acceleration5.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.

GlucoseHigh in DM.ElectrolytesNa-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.SerologyAutoAb,Antinuclear Ab, AntiGBM Ab, Hepatitis B,

HIV.Urine analysisRBC-Sediments GBN.,Pyuria-Interstitial nephritis.Spot urine collection for Total protein,creatinine

ratio.Normal-is <224 urine forTotal protein and creatinine clearance.Serum and urine protein electrophoresis.ECG,ECHO-LVH.

ImageXray Nephrocalcinosis.U.S.GSmall 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 emergency17mg/dl +pulmonary edema, fits, coma,

metabolic acidosis, hyperkalemia, deathTo 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 catheters.

Hello Kidney _YOU Are a KIDKID NEEWe will take care of you by modifying the

risk factors, And by retarding the progression,,,,,,.

Physicians.

THANK YOU

THANK YOU