B Metabolic wastes begin to accumulate Increased BUN and creatinine Stage II: Renal Insufficiency GFR 20 50 %

Increased Acid excretion and bicarbonate reabsorption to maintain normal pH

Decrease responsiveness to diuretics

Oliguria and Edema

Further glomerular damaged

Stage III: Renal failure GFR 10 20 %

C Loss of non-excretory renal function Loss of excretory renal function Stage IV: End Stage Renal Disease GFR <10 %

Increase

production of erythropoetin Alteration in cognitive process Impaired insulin function Changes in fat metabolism Immune disturbance Reproductive system

Trouble concentrating Glucose intolerance Increased triglyceride, total cholesterol and LDL Risk for Infection Sex hormone disturbance

Erratic blood glucose levels Anemia and pallor Decreased hemoglobin and hematocrit Decreased RBC s Fatigue Risk for Atherosclerosis Failure to convert inactive form of calcium D Decrease libido

Decreased excretion of nitrogenous wastes Decreased Na reabsorption in tubules Decreased potassium excretion Decreased phosphate excretion Decreased H excretion Loss of excretory renal function C

Hyperphosphatemia Metabolic Acidosis

Increased serum BUN and Crea Water retention Increased serum K level Hyperkalemia

Decreased Calcium absorption

Pruritus Fluid volume excess

Decreased serum Calcium level

(Hypocalcemia)

Increased workload of the heart Increase BP Generalized Edema (Anasarca)

Stimulate release of PTH

Minimal pleural effusion in the right side Cardiomegaly Pitting Edema

Increased absorption of Calcium from bones to blood

Sleep disorders

Risk for bone problems (osteoporosis, osteomalacia, renal osteodysthrophy) Unable to sleep in supine position

B Unaffected nephrons are damaged Increased glomerular pressure and the pressure in unaffected nephrons Unaffected nephrons overwork to compensate for the affected nephrons Renal function is reduced but no accumulation of metabolic wastes Stage 1: Diminished Renal Reserve GFR 50% Decrease GFR Impaired Blood Flow A A Prolonged increase pressure Kidneys do not recognize the increase in BP and continue to release renin Increase BP and Na absorption Angiotensin II cause vasoconstriction and stimulate Adrenal cortex to release Aldosterone Angiotensin I goes to the lungs and converted to Angiotensin II by Angiotensin converting enzyme Rennin converts angiotensionogen into Angiotensin I Release of renin Stimulation of RAAS Increase Na in Urine Polyuria / Nocturia Decreased reabsorption of Na Glumerolosclerosis Thickening of the small vessels Increase BP damages the

glomerular capillaries Predisposing Factors . Family History of Diabetes Mellitus and Hypertension Precipitating Factors . Lifestyle: Smoking, Drinking Alcohol . Disease: HTN, DM, recurrent infections