Renal failure
Inability of the kidneys to excrete wastes, concentrate urine and conserve electrolytes
Acute renal failure is abrupt in onset and often is reversible
Chronic renal failure develops slowly and is the end result of irreparable damage to the kidneys
Acute renal failure
Mortality rates are high
Azotemia is a common indicator
- an accumulation of nitrogenous wastes (urea nitrogen, uric acid, creatinine) in the blood.
Prerenal, intrarenal or postrenal
Prerenal
Due to impaired blood flow
Predisposes tubular necrosis
Causes:
Hypovolemia (hamorrhage, dehydration, excesive loss of
gastrointestinal tract fluids or fluid due to burn injury)
Septicemia
Heart failure or cardiogenic shock
Surgery or other interruptions to blood flow
Prerenal
ACE inhibitors reduce effects of renin on renal blood flow
NSAIDs reduce renal blood flow through inhibition of prostaglandin synthesis
Blood flow < 20% of normal causes ischemic changes to tubular epithelial cells
GFR decreased, little or no urine
BUN : creatinine ratio rises (15-20:1)
Intrarenal
Categorised according to site:
Tubular
Interstitial
Glomerular
Causes: actue tubular damage due to ischemia, the nephrotixic effects of durgs, tubular obstruction, toxins from a massive infection.
Acute tubular necrosis
Acute glomerulonephritis
Acute pyelonephritis
Acute tubular necrosis
Four phases:
Onset
Oliguric or anuric phase
Diuretic phase
Recovery
Onset
Time from onset of the precipitating event (eg. Ischemic phase of prerenal failure or toxin exposure) until tubular injury occurs
Oliguric phase
Usually a decrease in urine output
Oliguria (< 400 ml/day) most common in post ischemic forms
Nonoliguria (> 400 ml/day) more common in toxic tubular necrosis
When it occurs, begins shortly after the initiating event and lasts an average of 10 - 14 days
Oliguric phase
Nonoliguric may have a better prognosis than oliguric
Sudden retention of endogenous metabolites
Fluid retention gives edema, water intoxication and pulmonary congestion
If prolonged, hypertension frequently develops accompanied by uremia
Hyperkalemia is usually asymptomatic until levels rise above 6.0 - 6.5 mEq/l
ECG changes and muscle weakness
Diuretic phase
Begins within a few days to 6 weeks after oliguria
Excretion is now possible, but not completely regulated
Watch fluid and electrolyte levels
Recovery
Renal function recovers slowly
GFR returns to 70 - 80% of normal within 1 to 2 years
Postrenal
Obstruction of urine outflow from kidneys
Ureter - calculi and strictures
Bladder - tumours or neurogenic bladder
Urethra - prostatic hyperplasia
Chronic renal failure
Progressive and irreversible destruction of kidney structures
Causes:
Uncontrolled hypertension
Urinary tract obstruction and infection
Hereditary defects of the kidneys
Disorders of the glomeruli
Systemic diseases such as DM and SLE
Chronic renal failure
Progressive deterioration of filtration of glomerular filtration, tubular absorptive capacity, and endocrine function of the kidneys.
Signs grow insidiously and aren’t apparent until condition is well advanced
Stages
Diminished reserve
GFR approximately 50% 120-130mL/min, 1.73mL/min normal
Usually asymptomatic
Renal insufficiency
GFR down to 20 - 50%
Azotemia, anemia and hypertension
One of the earliest symptoms is polyuria with almost isotonic urine
isosthenuria; polyuria with urine that is almost isotonic with
plasma.
Stages
Renal failure
GFR < 20%
Edema, metabolic acidosis and hypercalcemia
End stage renal disease
GFR < 5%
Reduction in renal capillaries and scarring in glomeruli
Atrophy and fibrosis, size of kidney reduced
From your knowledge of how the kidney works, you should be able to fill in the mechanisms by which chronic renal failure would cause each of the problems listed below. How could chronic renal failure lead to:
A. Azotemia : The damaged glomerular reduce the amount of blood the kidney is able to filter. Therefore, the nitrogenous was in the blood is increased.
B. Metabolic acidosis : Kidney damage to glomeruli, which reduces amount of blood which is filtered, also reduces the amount of H+ ions excrete through the kidneys.
C. Hyperparathyroidism : The kidneys cannot activate vit D so calcium levels drop, which causes to increase in parathyroid hormone levels to mobilize Ca from bones. Continued over-stimulation of the parathyroid hormone results in hyperparathyroidism.