Chronic kidney disease

1. Chronic Kidney Disease
Dr. Debashis Priyadarshan Sahoo
PGT, First year
Department of General medicine
NEIGRIHMS

2. Definition:
• CKD is defined as abnormalities of kidney structure or function,
present for >3 months, with implications for health.
• Classified based on cause, GFR category, and albuminuria category.

3. Pathophysiology of CKD:
• Mechanisms of Damage
 Initiating mechanisms specific to
the underlying etiology
 Set of progressive mechanisms
(hyperfiltration and hypertrophy)

4. GFR:
• GFR peaks during the 3rd decade of life (120 mL/min per 1.73 m2)
• Annual mean decline in GFR is 1mL/min per year
• At age 70, GFR mean value becomes 70mL/min
• Mean GFR is lower in women than in men
• Albuminuria
• 24-hour urine collection – standard
• Spot first morning urine
• Males - >17mg of albumin per gram of creatinine
• Females - >25mg of albumin per gram of creatinine

5. GFR estimation:

6. Staging of CKD:
GFR category GFR Terms
G1 >90 Normal or high
G2 60-89 Mildly decreased
G3a 45-59 Mild to moderately decreased
G3b 30-44 Moderate to severely decreased
G4 15-29 Severely decreased
G5 <15 Kidney failure

7. RiskFactors
1. Hypertension
2. Diabetes mellitus
3. Autoimmune disease
4. Older age
5. African ancestry
6. Family history of renal disease
7. Previous episode of acute kidney injury
8. Presence of proteinuria
9. Abnormal urinary sediment
10. Structural abnormalities of the urinary tract

8. Clinical Abnormalities in Uraemia
Fluid and electrolyte
disturbances
Volume expansion
Hyponatremia
Hyperkalaemia
Hyperphosphatemia
Endocrine-metabolic
disturbances
Secondary hyperparathyroidism
Adynamic bone
Vitamin D–deficient
osteomalacia
Carbohydrate resistance
Hyperuricemia
Hypertriglyceridemia
Increased Lp(a) level
Decreased high-density
lipoprotein level
Protein-energy malnutrition
Impaired growth and
development
Infertility and sexual dysfunction
Amenorrhea
2-Microglobulin–associated
amyloidosis
Neuromuscular disturbances
Fatigue
Sleep disorders
Headache
Impaired mentation
Lethargy
Asterixis
Muscular irritability
Peripheral neuropathy
Restless legs syndrome
Myoclonus
Seizures
Coma
Muscle cramps
Dialysis disequilibrium syndrome
Myopathy
Cardiovascular and pulmonary
disturbances
Arterial hypertension
CHF
Pericarditis
HCM and DCM
Accelerated atherosclerosis
Hypotension and arrhythmias
Vascular calcification
Dermatologic disturbances
Pallor
Hyperpigmentation
Pruritus
Ecchymoses
Uremic frost
Gastrointestinal disturbances
Anorexia
Nausea and vomiting
Gastroenteritis
Peptic ulcer
Gastrointestinal bleeding
Peritonitis
Hematologic and immunologic
disturbances
Anemia
Lymphocytopenia
Bleeding diathesis
Increased susceptibility to
infection
Leukopenia
Thrombocytopenia

9. Leading categories of etiologies of CKD
• Diabetic glomerular disease
• Glomerulonephritis
• Hypertensive nephropathy
• Primary glomerulopathy with hypertension
• Vascular and ischemic renal disease
• Autosomal dominant polycystic kidney disease
• Other cystic and tubulointerstitial nephropathy

10. SodiumandWaterHomeostasis
• Total-body content of sodium and water is
modestly increased
• Dietary intake of sodium > urinary
excretion
PotassiumHomeostasis
• Hyperkalaemia
1. Increased dietary potassium intake
2. Protein catabolism
3. Haemolysis
4. Haemorrhage
5. Transfusion of stored red blood cells
6. Metabolic acidosis
7. ACE, ARBS and spironolactone

11. MetabolicAcidosis
• Less ammonia is produced
• Less protons is excreted

12. Treatment:Fluid,Electrolyte,andAcid-Base
Disorders
1. Adjustments in the dietary intake of salt
2. Loop diuretics
3. Renal replacement therapy
4. Avoidance of K in diet
5. Avoidance of K supplements and K-retaining medications
6. Kaliuretic diuretics
7. Sodium bicarbonate

13. Anemia:
Causes of anemia in CKD:
1. Relative deficiency of erythropoietin
2. Diminished red blood survival
3. Bleeding diathesis
4. Iron deficiency
5. Hyperparathyroidism / BM fibrosis
6. Chronic inflammation
7. Vitamin B12 and folic acid deficiency
8. Hemoglobinopathies
Treatment:
1. Recombinant human EPO
2. Modified EPO products
3. Blood transfusion
4. Iron supplementation

14. Management of anemia in CKD:

15. Abnormal hemostasis:
Causes:
• Prolonged bleeding time
• Decreased activity of platelet
factor III
• Abnormal platelet aggregation
and adhesiveness
• Impaired prothrombin
consumption
Treatment
• Desmopressin
• Cryoprecipitate
• Blood transfusion
• EPO therapy

16. Bone Manifestations ofCKD
• Hyperparathyroidism stimulates bone turnover - osteitis fibrosa cystica (Brown
tumour)
• Bone pain and fragility
• Compression syndromes
• Erythropoietin resistance
• The pathophysiology of secondary hyperparathyroidism and the consequent
high-turnover bone disease is related to abnormal mineral metabolism
1. Declining GFR leads to phosphate retention
2. The retained phosphate stimulates increased synthesis of PTH and growth of parathyroid
gland mass
3. Decreased levels of ionized calcium also stimulate PTH production.

17. • Vitamin D deficiency and osteomalacia.
• Calciphylaxis – heralded by livedo reticularis → patches of ischemic
necrosis
• Treatment:
1. Low phosphate diet
2. Phosphate-binding agents (calcium acetate, calcium carbonate)
3. Calcitriol

20. Cardiovascular abnormalities:
Abnormalities:
• Leading cause of morbidity and
mortality
• Ischemic Vascular Disease
• Heart failure
• Hypertension and LVH
Management:
• Lifestyle change
• Salt restriction – first line of therapy
• Management of Hypertension
• to slow the progression of the kidney
disease itself
• to prevent the extrarenal
complications of high blood pressure
• ACE inhibitors
• ARBs

21. Management of blood pressure:

22. Neuromuscular manifestations:
• Central nervous system (CNS), peripheral, and autonomic neuropathy
• Abnormalities in muscle structure and function
1. Early manifestations : Memory and sleep disturbances
2. Late manifestations : Neuromuscular irritability
3. Advanced : Asterixis, Myoclonus, Seizure, Coma

23. Gastrointestinal abnormalities:
• Uremic fetor
• Dysgeusia
• Gastritis, PUD and mucosal ulcerations
• Constipation
• Anorexia, nausea, vomiting

24. Investigations:
• ABG
• CBC
• Kidney function test
• Chest Xray PA view
• Serum uric acid, Phosphate, Vitamin D3 and PTH
• Serum Iron, Ferritin, Vitamin B12, Folic acid
• Urinalysis
• Serum albumin levels
• Lipid profile
Evidence of Renal-bone
disease:
1. Serum phosphate
2. 25-hydroxyvitamin D
3. Alkaline phosphatase
4. Intact PTH levels

25. Other tests:
Blood investigations
1. Serum and urine protein electrophoresis
2. ANA, anti DS DNA
3. Complement levels
4. C-ANCA, P-ANCA
5. Anti-GBM
6. Hepatitis B and C
7. HIV
8. VDRL
Imaging
• Renal ultrasonography
• Retrograde pyelography
• CT scan
• MRI
• Renal radionuclide scanning
• Biopsy

26. Treatment:

27. Treatments:
Stage 3 and 4 (Treating complications)
Stage 1 and 2
• No presenting symptoms due to decreased
GFR.
• Follow up.
• Complications become more prominent
• Anemia – easy fatigability
• Decreasing appetite
• Abnormalities in calcium, phosphorous
and mineral regulating hormones
• Abnormalities in Na, K, water and acid-
base homeostasis

28. • Stage 5:
1. Uremic syndrome
2. Renal replacement therapy is needed