Division of Natural Sciences
Lewis-Clark State College
Chapter 36: Alterations of Renal and Urological Systems
I. Nephron Function
A. Glomerular filtration -- blood pressure forces water and blood components into Bowman’s Capsule. This fluid is the filtrate. Filtration is pressure dependent and is determined by the net affect of 3 different pressures:
GBHP -- glomerular blood hydrostatic pressure
BOP -- blood oncotic pressure
CHP -- capsular hydrostatic pressure.
GBHP favors filtration; BOP and CHP oppose filtration.
PEFF = GBHP - (CHP + BOP)
PEFF (effective filtration pressure) is affected by some forms of kidney disease which change glomerular permeability. PEFF is also affected by changes in BOP as seen in renal diseases and liver diseases and by increases in CHP.
B. Tubular reabsorption - primary job of PCT. Reabsorption is selective, depends on osmosis, diffusion, active transport, and facilitated transport; regulated by hormones -- ADH and aldosterone.
C. Tubular secretion - primary function of DCT, collecting tubule, and collecting duct. Important for the regulation of serum pH. Other substances which are secreted are K+ and various drugs including penicillin and morphine.
II. Tests of Normal Renal Function
A. Plasma creatinine (Pcr)
Creatinine - product of muscle metabolism. Decreased GFR
results in increased PCR.
B. Blood urea nitrogen (BUN)
Urea formed from protein, a.a. degradation. Urea is filtered by the glomerulus. Decreased GFR results in increased BUN.
Both tests are used to assess GFR. Azotemia = increased BUN and PCR.
III. Glomerular Disorders
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commonly the result of immune reactions |
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in general, characterized by decreased GFR |
A. Glomerulonephritis (GN)
1. acute
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post-strep infection (either skin or throat); 1-3 wks following |
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Type III hypersensitivity reaction. |
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Inflammation increases permeability. |
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Glomeruli cells proliferate - glomeruli are blocked. |
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Manifestations: decreased GFR, edema, HTN, proteinuria, hematuria. |
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Inflammation subsides in 10-14 days |
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Normal kidney function returns in a few weeks to months later. |
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90% of children have complete recovery. |
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30-50% of adults may progress to other types of GN. |
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In some cases many glomeruli are completely destroyed. |
Pictured below on left a normal glomerulus. On the right is a glomurulus is blocked.
2. chronic
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slow, progressive destruction of the glomeruli from long-standing GN. |
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many glomeruli are completely replaced by fibrous tissue leading to loss of nephron function. |
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may be a de novo disease. |
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manifested by proteinuria, HTN, azotemia, uremia. |
B. Nephrotic Syndrome. (NS) (excretion of 3.5 g (or more) of protein/day.)
1. pathophysiology
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increased permeability of glomerular membrane -- any disease that causes this can result in NS. |
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caused by chronic GN and other types of glomerular disorders. |
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Decreased plasma proteins decreases BOP (may fall from 28 to 6 mm Hg). |
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Edema, decreased blood pressure (as fluid is lost to interstitial spaces) |
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increased angiotensin, aldosterone, and ADH leads to Na+ and water reabsorption which in turns increases the edema. |
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up to 20g of protein lost/day. |
2. clinical manifestations
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proteinuria, edema (up to 40 extra liters; 15L in ascites) |
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hyperlipidemia - maintains osmolarity |
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Vit. D deficiency - 25 hydroxycholecalciferol normally bound to globulin - lost with urine, decreased Ca++ absorption by g.i. tract. |
IV. Renal Failure.
A. Classification of renal dysfunction.
Stage I - decreased renal reserve; normal PCR, BUN. Impairment seen only with high demands.
Stage II - renal insufficiency - decrease in renal function to 25%; slight increase in BUN and PCR; symptoms of polyuria and nocturia appear with loss of concentrating ability; loss of normal diurnal pattern of increased concentrating ability at night.
Stage III - End-stage renal failure. Less than 10% of renal function. Uremia occurs. (Uremia – azotemia and all of the metabolic changes that affect every system in the body.)
B. Types of renal failure.
1. acute - abrupt decrease in renal function; azotemia,
oliguria (< 400ml/day); can be reversed frequently with early treatment.
a. pathophysiology
1. pre-renal acute failure (circulatory renal failure).
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caused by impaired renal blood flow |
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hypovolemia, hypotension |
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shock (cardiogenic, septic) |
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pulmonary embolism ( decreases CO) |
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renal stenosis (most commonly from atherosclerosis) |
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can lead to ATN |
2. intra-renal acute failure (intrinsic)
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glomerulonephritis |
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DIC |
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ATN (acute tubular necrosis) – most common cause of intra-renal acute failure. |
(Acute tubular necrosis -- caused by ischemia from shock, HTN, renal poisons such as Hg ions, carbon tetrachloride, and antibiotics such as gentamicin. These agents cause necrosis of tubular epithelium and the epithelial cells slough off and block the renal tubules. CHP increases and PEFF decreases.)
3. post-renal acute failure -urinary tract obstruction:
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prostatic hypertrophy |
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urethral obstruction |
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ureter obstruction |
b. clinical manifestations - 3 phases
1. oliguria phase: azotemia; water, Na+ retention, edema, HTN (increased by 20-40 mm Hg), uremia (nausea, vomiting, acidosis) duration depends on cause; lasts 7-10 days in ATN.
2. diuretic stage: urine output>400ml/day; generally lasts 2-3 wks; osmotic diuresis by high BUN and impaired ability of renal tubules to conserve Na+ and water. Pt may develop K+, Na+, water deficits; may cause death.
3. recovery: 3-12 mons; 30% never fully recover; ATN - 50% mortality; 66% die during oliguria, 34% die during diuretic.
c. treatment
dialysis
correct fluid and electrolyte imbalance
maintain nutrition
low protein diet (decreases BUN).
2. chronic renal failure: large number of nephrons are destroyed; kidneys adapt; no symptoms until GFR = 25% on normal.
a. causes
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chronic GN |
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diabetic nephropathy |
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renal vascular disease (atherosclerosis) |
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pyelonephritis |
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benign nephrosclerosis |
b. pathophysiology
1. abnormal nephron function: with loss of nephrons, remaining nephrons hypertrophy: 50-100% increase in blood flow, increased GFR, solute load, and tubular reabsorption. These compensatory mechanisms maintain until 75% of nephrons are lost. After this point, functional nephrons lose ability to [ ] or dilute urine; specific gravity of urine becomes fixed and = to that of the filtrate (isthoneuria). This causes the polyuria/noctura seen in early CRF. As loss of nephrons continues, eventually oliguria develops as well as azotemia and uremia.
2. effects on body water/electrolytes
a. water - loss of ability to concentrate or dilute urine, increased vulnerability to water imbalance;
excessive intake > edema, CHF
diarrhea, vomiting > dehydration
b. Na+ :
during polyuria stage - Na+ wasting
during end-stage - Na+ retention and concomittant water retention, edema, HTN, heart failure.
c. K+ - end-stage oligura:
hyperkalemia, decreased secretion by renal tubules/dysrhythmias
d. H+:
decreased H+ secretion, acidosis, Kussmaul respiration, contributes to hyperkalemia.
e. Ca++ and phosphate:
impaired synthesis of 1,25 dihydroxycholecalciferol;
decreased Ca++ absorption by g.i. system (osteomalacia).
Decreased GFR> hyperphosphatemia
HPO4 = binds with Ca++ >> CaHPO4
Deposits in soft tissues such as the cornea, heart, lung, and kidney.
Decreased Ca++ stimulates release of PTH
Calcium loss from bones and replacement with fibrous tissue (osteitis fibrosa).
3. azotemia:
urea, uric acid, creatinine accumulate. [urea] increases to 10X normal w/in 1- 2 wks of renal failure.
4. anemia:
decreased erythropoietin,
increased toxins
dialysis
c. clinical manifestations - uremia
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accumulation of toxins: anorexia, nausea, vomiting, diarrhea. |
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neurological changes: encephalopathy; fatigue, decreased attention, coordination. Uremic coma from acidosis, toxins, hyperkalemia. |
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HTN, edema, CHF, pulmonary edema. |
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Immunological suppression |
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Kussmaul respiration |
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Change in skin color - accumulation of urinary pigments. |
d. treatment: dietary management
hemodialysis
