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Pathophysiology of Chronic Renal Failure: By: Jonnel Montoya Musngi BSN 4-B

Chronic kidney disease can result from conditions that damage the kidneys over time such as diabetic nephropathy, chronic glomerulonephritis, chronic pyelonephritis, and polycystic kidney disease. As kidney function declines, waste products accumulate in the bloodstream leading to complications. Early stages involve hypertrophy of remaining nephrons but later stages see a continuous decline in renal function with scarring of glomeruli and atrophy of the kidney. End stage renal disease occurs when kidney function declines to less than 10% and the body is no longer able to maintain fluid, electrolyte, and acid-base balance without dialysis or transplantation.

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Kenrick Randell Ibana
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250 views1 page

Pathophysiology of Chronic Renal Failure: By: Jonnel Montoya Musngi BSN 4-B

Chronic kidney disease can result from conditions that damage the kidneys over time such as diabetic nephropathy, chronic glomerulonephritis, chronic pyelonephritis, and polycystic kidney disease. As kidney function declines, waste products accumulate in the bloodstream leading to complications. Early stages involve hypertrophy of remaining nephrons but later stages see a continuous decline in renal function with scarring of glomeruli and atrophy of the kidney. End stage renal disease occurs when kidney function declines to less than 10% and the body is no longer able to maintain fluid, electrolyte, and acid-base balance without dialysis or transplantation.

Uploaded by

Kenrick Randell Ibana
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOC, PDF, TXT or read online on Scribd
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Diabetic Nephropathy

Chronic Glomerulonephritis

Chronic Pyelonephritis

Pathophysiology of Chronic Renal Failure


Non-modifiable Risk Factors: Age Gender Heredity Modifiable Risk Factors: Diet Sedentary Lifestyle Nephrotoxins

Polycystic Kidney Dse.

HPN

Systemic Lupus Erythematosus

Intracellular Glucose Repeated Inflammation

Multiple Bilateral Cysts

Long Standing HPN leads to further arteriosclerosis

Supports the formation of abnormal glycoprotein in the basement membrane of glomerulus

Ischaemia, Nephron loss, Shrinkage of Kidney Stage

Renal Blood Renal Reserve Damage to Nephrons 50% damage More than 75% damage Renal Insufficiency As nephrons are destroyed, the remaining nephrons undergo changes to compensate for those Remaining nephrons must filter more solute particles from the Hypertrophy of remaining nephrons Nephrons cannot tolerate the work Further damage of nephrons 80-90% damage Renal Failure Impaired kidney function & Uremia GFR 20-50% BUN, Creatinine GFR 50% Normal BUN, Creatinine

As cysts fill, enlarge & multiply, kidneys also enlarge Renal blood vessels & nephrons are compressed & obstructed & functional tse. are destroyed Renal Parenchyma atrophies & become fibrotic & scarred

Production of large variety of auto antibodies against normal body components such as nucleic acids, RBC, platelet, and WBC SLE antibodies react with their corresponding antigen

Glomerulosclerosis impairs the filtering fxn. of the glomerulus thus protein lost in urine

Forms Immune Complexes

Deposited in the connective tse. such as blood volume & kidneys

Stage

Trigger an inflammatory response and damage the kidney

Stage

GFR 10-20% Sharp BUN,

Na & H2O retention

K retention
+

HCO3 production in kidney

H retention
+

Urine Output Oliguria

Blood

Hyperkalemia Metabolic Acidosis Lungs Compensates Kussmauls Respiration

Nitrogenous waste impairs platelets GI stress

Erythropoietin production

Mg retention
+

Vit. D activation

Phosphate retention Hyperphosphatemi Ca+ absorption

Continuous decline in renal fxn. > 90% kidney Reduction in renal capillaries Scarring of Glomeruli Atrophy & Fibrosis of Stage End Stage Renal Dse. (ESRD) Continuous Multisystem Affectation Death

Bleeding tendencies

Hypermagnesemia Anemia

Toxins irritate pericardial sac Pericarditi Cardiac Tamponade

Toxins impair WBCs, humoral & cell mediated immunity; Fever is suppressed; Phagocyte becomes defective

Salivary urea breakdown Uremic Fetor

Deposit of urea on skin Uremic Frost Yellowish hue

Toxins affect the nerve fibers Atrophy & Demyalination Peripheral Neuropath Restless Leg Syndrome

Toxins causes CNS affectation Uremic Encephalopathy Reduction in alertness & awareness Changes in mentation Difficulty of concentrating Fatigue Insomnia Psychiatric symptoms

Retentio n of Cells become resistant to insulin Erratic blood glucose level Because of glucose intracellularly, liver produces tryglycerides & HDL

Malfunction of RAAS

GI bleeding

Blood loss during hemodialysis

Hypocalcemia Parathyroid overworks (Hyperparathyroidism) PTH secretion Ca+ resorption from bone + Ca absorption from GI tract Renal Osteodysthrophy Osteomalacia Osteoporosis Bone tenderness Bone pain Muscle Weakness

Immune System Decline Risk for Superinfection

Irritation of Phrenic Hiccups

Edema

Heart Failure

Anorexia Nausea Vomiting Gastroenteritis Peptic Ulcer

Loss of appetite Fatigue Weakness Pallor

GFR less than 10%

Pulmonary Edema Peripheral Edema

Atherosclerosis

Thrombus & Embolus Formation

By: Jonnel Montoya Musngi BSN 4-B

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