Chronic kidney disease is a progressive loss of kidney function that results in the buildup of waste products and fluids in the body. The main causes are diabetes, hypertension, and glomerular diseases. Symptoms include changes in fluid balance like edema, electrolyte imbalances, and accumulation of waste products that can damage multiple organ systems. Treatment focuses on controlling blood pressure and protein levels to slow disease progression, along with managing complications like anemia and bone disease. End-stage renal disease occurs at a glomerular filtration rate below 15 mL/min/1.73m^2 and requires renal replacement therapy like dialysis or kidney transplant.

1. Chronic kidney disease
• Dr.B.Mounika
• Dept of General Medicine

2. Introduction
Etiology
Pathogenesis
Diagnosis
Complications
Management

3. Chronic kidney disease (CKD) :
CKD is a progressive, irreversible deterioration in renal function in
which the body’s unable to maintain metabolic And fluid and electrolyte
balance resulting in uremia or azotemia.
Other names-CRF,CRD..
Azotemia: It is biochemical abnormality i.e elevation of blood urea
nitrogen(BUN) and serum creatinine.
Uremia :Syndrome that incorporates all signs and symptoms seen in
various systems throughout the body caused by raised
BUN,Cr,Acute/chronic Renal failure.

4. • ETIOLOGY AND RISK FACTORS
o Decreased renal blood flow
o Systemic diseases
 Diabetes mellitus
 Hypertension
 SLE
 Polyarteritis
 Sickle cell disease
 Amyloidosis
 Cc giomerulonephritis
 Pyelonephritis
 Arf

5. o Obstruction of the urinary tract
o Hereditary lesions
Polycystic kidney disease
o Infections
o Vascular diseases
o Medication or toxic agents
o Environmental or occupational agents
Lead
Cadmium
Mercury
Chromium

6. Most common causes:
 Diabetes
 Hypertension
 Glomerular diseases
 Systemic diseeases
 Interstitial diseases
 Unknown

7. Pathogenesis:

8. Clinical manifestations:
• Urinary symptoms:
Polyuria results from inability of kidneys to concentrate urine,Occurs most
often at night
Oliguria,
Anuria Occurs as CKD worsens

9. Alterations in fluids and electrolytes:
 Sodium & Water retention- PITTING EDEMA in the lower extremity
 Fluid accumulation -Pulmonary edema and loss of air space-
Ventilation-perfusion mismatch –SOB
 Hyperkalemia-Malaise, palpitations, arrhythmias..
 Hyperphosphatemia
 Hypocalcemia
 Altered CHO metabolism
 Elevated triglycerides
 Waste products accumulation-BUN ↑ and serum creatinine levels ↑ as
GFR ↓

10. Metabolicacidosis:
 Impaired H+ secretion from the body leads to anion-gap
metabolic acidosis.
 In tubulo-interstitial disease or diabetic nephropathy causes
Non-anion-gap renal tubular acidosis.
 Protein energy malnutrition –WT LOSS

11. Hematologic system:
Anemia:Fatigue, reduced exercise capacity, and pallor
Bleeding tendencies:
Defect in platelet function.
Infection:
Changes in leukocyte function
Altered immune response and function
Diminished inflammatory response

12. Renalosteodystrophy: Increased risk of fractures
 Hypocalcemia :
Early stages due to hyperphosphatemia
Later stages due to decreased synthesis of 1α-hydroxylase vitD
 Sec/Ter HyperPT: Occurs due hyperphosphatemia
…Osteoporosis,Osteomalacia,Calcium deposition in soft tissue
Complications of uremia:
Urea and other toxins accumulate in the blood and cause life threatening
issues
 Uremia-induced platelet dysfunction-Increased tendency to bleed and
ecchymosis, GI bleeding
 Uremic pericarditis-Chest pain, malaise, Pericardial friction rub
 Uremic encephalopathy-Headaches, confusion, coma

13. CVS:Hypertension,Heart failure,Left ventricular hypertrophy,Peripheral
edema,Dysrhythmias,Uremic pericarditis.
CNS:Altered mental ability,Seizures and Coma. Dialysis
encephalopathy,Peripheral neuropathy.
GIT:N/V ,Mucosal ulcerationsStomatitis Uremic fetor (urinous odor of
the breath)GI bleedingAnorexia.
RS:Kussmaul respiration,DyspneaPulmonary edema,Uremic
pleuritis,Pleural effusionPredisposition to respiratory infections,Depressed
cough reflex,“Uremic lung.

14. Stages and Complications of CKD

15. Investigations :
History and physical examination
Routine lab measurements
• BUN
• Serum Creatinine
• Serum Electrolytes
• Hematocrit and Hb levels
• Urine Analysis
• Urine Culture
 Identification of Reversible Renal Disease
• Renal Ultrasound
• Renal Scan
• CT Scan
• Renal Biopsy

16. Usg findings in CKD:
 Increased parenchymal echogenecity
 Loss of corticomedullary differentiation
 Bilateral small kidney <10cm

17. Treatment:
Aim of treatment
 Prevention of further deterioration
 Treatment of complications
Controlling Blood Pressure,Sugar,Proteinuria are key elements in
the reduction of CKD progression.

18. • Hypertension :
Target BP (120-140SBP/70-90DBP)depends on GFR,Proteinuria
Antihypertensive drugs:
 First-line Agents- ACEI,ARB
 Second-line Agents-Diuretics(thiazide OR furosemide)
 Third-line Agents-CCB(diltiazem, verapamil, amlodipine, diltiazem),BB
(labetalol )
Sodium restriction-Diets vary from 2 to 4 g depending on degree of
edema and hypertension

19. • Proteinuria:
ACEI,ARB should be advised to all patients with diabetic
nephropathy and patients with CKD and proteinuria, irrespective of
whether or not hypertension is present.
ACEI,ARB reduces proteinuria by reducing BP, glomerular
perfusion pressure and GFR
Protein restriction:
0.6 to 0.75 gm/kg of ideal body weight/day
1.2 to 1.3 gm/kg of ideal body weight/day once the patient starts
dialysis

20. Hyperkalemia:
For mild hyperkalemia -K binding agents: Zirconium cyclosilicate and
Patiromer
For severe-
 IV insulin and glucose
 IV 10% calcium gluconate
 Sodium bicarbonate-Shift potassium into cells,Correct acidosis
 Sodium polystyrene sulfonate
 Avoid high-potassium foods -Oranges, Bananas,figs,
avocados,Tomatoes,Green vegetables
,milk,yoghurt,chocoliate,baked,fries,salt substitutes.
 Avoid drugs which cause hyperK-ACEI,ARB,K-sparing diuretic.

21. Anemia:
Erythropoietin:Epoetin alfa Administered IV or subcutaneously
Increases hemoglobin and hematocrit in 2 to 3 weeks.
Starting dosage 50-150 units/kg per week IV or SC, 1-3 times per wK
Side effect: Hypertension
Iron supplements:
If plasma ferritin <100 ng/ml
Folic acid supplements:
Needed for RBC formation
Avoid blood transfusions

22. Renal osteodystrophy :
• Phosphate intake restricted to<1000 mg/day
• Phosphate binders
1.Calcium carbonate-Bind phosphate in bowel and excreted
2.Sevelamer hydrochloride-Lowers cholesterol and LDLs
Phosphate binders Should be administered with each meal.
Phosphate restriction:1000 mg/day ,Foods high in phosphate Dairy products
• Supplementing vitamin D-
Ergocalciferol (D2)
Cholecalciferol(D3)
• Controle secondary hyperparathyroidism with
 Calcimimetic agents -Cinacalcet (Sensipar)
↑ Sensitivity of calcium receptors in parathyroid glands,decrease plasma PTH
 Vitamin D analogs
 Calcium based phosphate binders-Calcium acetate,Calcium carbonate
• Subtotal parathyroidectomy

23. Metabolic acidosis:
• plasma bicarbonate concentrations should be maintained above 22 mmol/L
• Sodium bicarbonate supplements given-starting dose of1 g 8-hourly OR
• NaHCO3 0.5–1.0 mEq/kg daily
• There is some evidence that correcting acidosis may reduce the rate of
decline in renal function.

24. Oral hypoglycemic drugs in CKD:
Contraindications:
1-Biguanide: Metformin if SCr1.5 mg/dLin men, 1.4 mg/dLin women”or
GFR 30 mL/min/1.73 m2
2-sulfonylureasTolazamide ,Tolbutamide, Acetohexamide and
Glyburide.Chlorpropamide if GFR 50 mL/min/1.73 m2.
3-Alpha-glucosidaseinhibitors
Acarbose if GFR 30 mL/min/1.73 m2
Miglitilol GFR 25mL/min/1.73 m2
Safe drugs ,can be used in dialysis pts –DPP4 inhibitors
Drugs need dose reduction in dialysis pts-Meglitinides

25. ESRD:
End-stage renal disease (ESRD) occurs when GFR <15ml/min
Renal Replacement Therapy (RRT)
required when the kidneys are functioning at less than 10–15%.
RRT is accomplished in one of the following ways:
1-Dialysis
Hemodialysis
Peritoneal dialysis
2-Kidney transplant

26. THANK YOU