Only for the beneficial of the students

1. CHRONIC KIDNEY
DISEASE/CHRONIC RENAL FAILURE
• Either kidney damage or a decreased GFR of less than 60 ml/min/1.73m ² for
3 or more months
• Divided into following stages
STAGE 1 Kidney damage with normal or increased GFR (>90ml/min/1.73 m²)
STAGE 2 Mild reduction in GFR (60-89 ml/min/1.73 m²)
STAGE 3 Moderate reduction in GFR (30-90ml/min/1.73 m²)
STAGE 4 Severe reduction in GFR (15-29 ml/min/1.73 m²)
STAGE 5
(ESRD)
Kidney Failure (GFR< 15ml/min/1.73 m²)or dialysis

2. • Stage 1& 2 cannot be diagnosed based on GFR ALONE
• GFR can be normal in these stages

3. ETIOLOGY
• PRIMARY GLOMERULAR DISEASES
• Focal& segmental Glomerulosclerosis
• Membranoproliferative Glomerulonephritis
• IgA Nephropathy
• Membranous nephropathy
• SECONDARY GLOMERULAR DISEASE
• Diabetic nephropathy
• Hypertension
• Amyloidosis
• Post –infectious glomerulonephritis
• HIV –associated nephropathy
• Collagen – vascular diseases
• Sickle cell nephropathy

4. TUBULOINTERSITIAL NEPHRITIS
• Drugs
• Heavy metals
• Analgesic nephropathy
• Reflux/chronic pyleonephritis
• Idiopathic
OBSTRUCTIVE NEPHROPATHIES
• Prostate enlargement
• Calculus
• Retroperitoneal fibrosis
• Tumor
VASCULAR DISEASES
Renal artery stenosis
Vascultis

5. HEREDITARY DISEASES
• Polycystic kidney disease
• Medullary cystic disease
• Alport’s syndrome

6. • Also known as Chronic Kidney Disease or Chronic Glomerulonephritis.
• Final stage of a variety of glomerular diseases resulting in irreversible impairment of renal
function.
• Conditions leading to ESRD
a. RPGN(90%)
b. Membranous GN(50%)
c. MPGN(50%)
d. FSGS(50%)
e. IgA nephropathy(40%)
f. Acute PSGN(1%)
g. Idiopathic(20%)

7. • Patients of chronic kidney disease on dialysis show a variety of dialysis associated changes
that include acquired cystic disease, occurrence of adenomas and adenocarcinomas of the
kidney, calcification of tufts and deposition of calcium oxalate crystals in tubules
• CLINICAL FEATURES
• FLUID & ELECTROLYTE IMBALANCE
• In most patients with stable CKD ,there is retention of sodium & water leading to fluid
overload
• Fluid overload manifests as peripheral edema, ascities, pleural and pericardical effusions
• Contributes to development of hypertension also
• Rarely hyponatremia is seen
• Responds to water restriction
• Hyperkalemia – potassium excretion is impaired
• Rarely Hypokalemia – result of renal potassium wasting in diseases c
• Fanconi’s syndrome
• Renal tubular acidosis
• Hereditary or acquired tubulointerstital diseases

8. ACID –BASE DISTURBANCE
• Metabolic acidosis – inability to excrete acid load due to less ammonia formation
in the kidney
• Severe metabolic acidosis – patient may have deep respiration
• Anorexia
• Nausea
• Vomiting
• Hiccoughs
• Pruritus
• Muscular twitching fits
• Drowsiness
• Coma

9. UREMIA
• Constellation of signs and symptoms seen in renal failure
Manifestation –anorexia
Nausea
Vomiting
Growth retardation
Peripheral neuropathy
CNS features – such as altered sensorium
Seizure
Coma
Bleeding – due to abnormal platelet adhesion & aggregation due to uremia
Pericarditis & Pericardial effusion – indication of dialysis

10. DISTURBANCES IN CALCIUM &
PHOSPHATE METABOLISM
• RENAL OSTEODYSTROPHY
• Kidney is the site of formation of 1-25 –dihydroxycholecalciferol (active Vit D)
• Diminished active Vit D formation in CKD leads to hypocalcemia &
hyperphosphatemia
• Hypocalcemia & Hyperphosphatemia – stimulate PTH production
• Increased PTH –stimulates bone turnover
• Leads to Osteitis fibrosa cyctica
• Characterized by marrow fibrosis & bone cysts

11. ANEMIA
Due to reduced renal erythropoietin production
• Normocytic & normochromic
• HYPERTENSION - due to volume expansion and /or activation of the renin –
angiotenin system
• DYSLIPIDEMIA & ATHEROSCLEROSIS –Abnormal lipid metabolism
• TG & Cholesterol levels are increased
• To the risk of atherosclerosis
• ENDOCRINE DYSFUNCTION
• GROWTH HORMONE- End –organ resistance to GH action
• Due to increased levels of insulin growth factor binding brotein
• Contributes to growth impairment especially in children

12. • GONADAL HORMONE –Abnormalities in gonodal hormones in both gender patient
• Result in delayed puberty
• 2/3 of adolesecents with ESRD
• Males –reduced testosterone
• - elevated LH &FSH
• Females – Reduced serum estrogen
• - elevated LH &FSH
- Loss of the LH & PULSATILE PATTERN
Results in annovulations
GROWTH IMPAIRMENT
Growth failure is common in childhood
Multifatorial
Due to metabolic acidosis
Decreased caloric intake
Renal dystrophy
Aletrations in growth hormone metabolism

13. INVESTIGATIONS
• Urea & creatinine are elevated
• Level of serum creatinine correlates with the degree of renal impairment
• Urine analysis –Fixed specific gravity of around 1.010
• WBc’s –Present in the urine in UTI
• Papillary necrosis
• BPH
• Renal tuberculosis
• Eosinophilic – Present in allergic tubulointersitial disease
• RBCs Cast – GN

14. • Serum Electrolytes- Hyperkalemia ,Hypocalcemia ,Hyperphosphatemia are seen
• Bicarbonate levels are reduced
• Anemia – Normocytic Normochromic
• ultrasound abdomen – Bilateral small sized kidneys
• Rule out obstruction ,polycystic kidney disease
• Chest X –ray – s how pulmonary edema & pericardial effusion
• ECG – signs of Hyperkalemia or cardiac disease
• Renal artery Doppler – Renal artery stenosis is suspected
• Hepatitis B,C & HIV serology
• If dialysis is needed ( Vaccination against Hepatitis B If no previous infection
:isolation of dialysis machine if positive)
• ANA if connective tissue disease is suspected
• ANCA if vasculitis is suspected
• Renal biopsy to establish the diagnosis in selected area

15. MANAGEMENT
TREATMENT OF UNDERLYING CAUSE
• Cause of renal failure & institute treatment for that
• For eg, Control of diabetes, hypertension ,immunosuppression in GN
REVERSIBLE FACTORS IN CRF
• Hypertension
• Renal artery stenosis
• Hypovolemia
• Cardiac failure
• Urinary tract obstruction
• Urinary tract infection
• Infection
• Nephrotoxic drugs

16. • SLOWING THE PROGRESSION OF CKD
• ACE inhibitors
• Monitor Creatinine & potassium after starting on ACE inhibitors
• Can be worsening of GFR & Hyperkalemia
• Angiotensin II receptor antagonists also have similar effect
• Restriction of dietary protein intake also delays the progression of CKD
• TREATMENT OF THE COMPLICATIONS OF RENAL FAILURE
• ANEMIA –Recombinant human erythropoietin is effective in correcting the
anemia of CRF
• Severe anemia should be corrected by blood transfusion
• Volume overload – Should be treated by a combination of dietary sodium
restriction & diuretic therapy, usually with a loop diuretic given daily
• HYPERKALEMIA –Avoid potassium rich foods such as coconut water, fruit juices,
etc
• Loop diuretics –frusemide to increase urinary potassium losses

17. • Potassium binding agents (Kayexalate 5 gm with each meal )
• Salbutamol nebulizations
• 50% dextrose 100ml with 10 units of insulin infusion 8th hour
• Will push the potassium into the cells & decrease serum potassium
• METABOLIC ACIDOSIS
• Sodium bicarbonate
• Sodium citrate
• HYPERPHOSPHATEMIA
• Treated by oral phosphate binders to maintain serum phosphorous levels less than
5mg/dl
• Calcium carbonate or calcium acetate –used as phosphate binder (risk of causing
hypercalcemia)
• Sevelamer – controls the serum phosphate concentration without inducing
hypercalcemia

18. RENAL OSTEODYSTROPHY - Treated by calcitriol and control of phosphate
levels
HYPERTENSION – Controlled by a combination of antihypertensives &
diuretics
ACE inhibitors or angiotensin II receptors blocker can be used initially if
creatinine is not high
Other Hypertensives are calcium channel blockers, clonidine, beta blockers &
Alpha blockers
ABNORMAL LIPIDS – Hypercholesterolemia is almost universal in patients
with significant proteinuria
Increased triglycerides levels are also common in patients
Can be controlled with HMG –CoA reductase inhibitors ( eg
,atorvastatin,rosuvastatin)
BLEEDING – Due to abnormal platelet function
Dialysis can partially correct the bleeding tendency

19. • RENAL REPLACEMENT THERAPY - Conservativ measures are
inadequate,hemodialysis must be planned
• Renal Transplantation can be considered in suitable patients