ePathoPlusPage
|
ePathoPlusPage
|
Renal Dysfunction
Outline
A. Review of Normal Renal Function.
1. Water Balance
a. renin angiotensin system (see diagram in Hypertension lecture)
b. ADH
c. polyuria = excessive urine
oliguria = decreased urinary output (<400 ml in 24 hrs)
anuria = no urinary output
2. Getting rid of metabolic waste
a. protein metabolism - urea nitrogen as waste product
1. BUN (measured in blood)- normal = 11-23 mg/dl
2. if elevated, then = azotemia
b. muscle metabolism - creatinine as waste product
1. normal creatinine levels = .6 - 1.2 mg/dl
3. Electrolyte balance
a. K+ (normal = 3.5 - 5.0 meq/l)
1. relationship between Na+, K+ and H+
b. Ca+ and PO4
1. when Ca+ is absorbed, PO4 is excreted and vice versa
4. Vitamin D metabolism
1. an enzyme found in kidney activates precursor of Vit D
5. Acid Base balance
1. renal tubules regulate plasma bicarbonate
2. metabolize and excrete acids
6. Blood pressure regulation
a. renin angiotensin
7. Red blood cell production
a. kidney synthesizes hormone erythropoietin
B. Classification of Renal Disease
1. Prerenal (poor kidney perfusion)
a. due to hypovolemia, cardiac failure, septic shock,
cirrhosis
b. urine Na+ decreased, sp. gravity increased, oliguria,
BUN elevated, creatinine normal
2. Renal (primary kidney pathology)
a. Glomerular
1. examples: acute and chronic nephritis, diabetic sclerosis,
lupus,
b. Vascular
1. examples: nephrosclerosis, vasculitis
c. Tubular
1. Acute tubular necrosis
d. Interstitial
1. examples: pyelonephritis, tuberculosis
e. Tumors or cysts
1. example: polycystic kidney disease
f. clinically- urine Na varies, BUN elevated, creatinine elevated,
sp. gravity varies
3. Postrenal (obstructive disorders)
a. examples: calculi, tumors, benign prostatic hypertrophy (BPH),
cancer, strictures or stenosis
C. Uremia
1. a syndrome caused by elevated levels of urea nitrogen in blood
2. symptoms:
a. nausea and vomiting
b. lethargy, altered sensorium
c. bleeding
d. pericarditis
e. pruritis
f. uremic frost (extreme conditions)
D. Nephrosis (Nephrotic syndrome)
1. syndrome of clinical findings:
a. massive proteinuria
b. lipiduria
c.hypoalbuminemia
d. generalized edema
e. hyperlipidemia (cholesterol > 300 mg/dl)
2. due to increased glomerular permeability to plasma proteins,
3. Causes of Nephrosis
| Pathology | Causes | |
| Minimal Change Disease | diffuse loss of foot processes from the epithelial layer of glomerular membrane (no sign renal dysfunction but increased susceptibility to infection with gram + bacteria, formation of emboli, hyperlipidemia and protein malnutrition) | peak age between 2- 6 yrs of age, occurs after hx of recent upper infections or receiving routine immunizations |
| Focal Sclerosis | sclerosis of some but not all glomeruli (presence of HTN and decreased renal function) | often idiopathic, but may be associated with heroin abuse, AIDS, or reaction to NSAID |
Membranoproliferative Glomerulonephritis
|
Basement membrane thickening and cellular proliferation. Two types I and II. Usually progresses to ESRD in few months or yrs | Immune etiology, 1/3 with Type I had hx of recent upper respiratory infection |
| Membranous Glomerulonephropathies | most common nephrosis in adults, 50- 60 yrs of age usual onset. Diffuse thickening of glomerular basement membrane due to deposition of immune complexes. (about 1/2 develop a slow but progressive loss of renal function) | idiopathic or assoc. with autoimmune disorders, infections, chronic hepatitis B, DM, thyroiditis, reaction to gold, PCN, captopril |
4. most cases of nephrosis (except membranoproliferative
glomerulonephritis) are successfully tx with corticosteroids
E.Nephritic Syndrome
1. characterized by hematuria with rbc casts, decreased GFR,
azotemia, oliguria and HTN
2. caused by inflammatory response of endothelial, mesangial or
epithelial cells of glomeruli, may be primary Dx (such as acute
proliferative glomerulonephritis or IgA nephropathy) or secondary to vasculits or lupus
3. Acute proliferative glomerulonephritis
1. caused by infection with group A beta hemolytic streptococci,
usually occurring in children
2. if to occur follows 10 days - 2 weeks following upper resp
strep infection
3. prognosis good if in children, worse if in adults
4. IgA nephropathy (Buerger's disease)
1. most common cause of acute glomerulonephritis in US
2. often preceded by upper resp tract infection, GI tract symptoms
or flulike illness
3. deposition of IgA in mesangium of glomerulus
4. becomes a chronic Dx with recurrent episodes of hematuria and
mild proteinuria, progression is slow, over several decades, fish
oil in diet may retard progress.
F. Acute Renal Failure
1. usually sudden, reversible
2. Acute Tubular Necrosis (ATN)- accounts for 75% of all cases of
acute renal failure. Two types:
a. toxic, due to exposure to radiographic contrast media, solvents,
heavy metals, antibiotics, pesticides
b. ischemic (more serious, worse prognosis). Occurs when perfusion to kidney is dramatically reduced
c. Clinical Picture (Three Phases)
1. Oliguric Phase (may last 8 - 14 days)
a. inability to excrete wastes
b. inability to regulate electrolytes
c. inability to excrete fluids (get fluid overload, edema
CHF, increased BP)
2. Diuretic Phase (lasts 48 - 72 hrs)
a. mobilization of fluids, increased urinary output
(danger of hypovolemia)
b. slowly excrete metabolic wastes
3. Recovery Phase
a. BUN and creatinine levels slowly return to normal
G. Chronic Renal Failure and End Stage Renal Disease (ESRD )
a. Stages of Progression
| Diminished Renal Reserve | GFR about 50% normal, no symptoms but increased risk of azotemia in response to drugs |
| Renal Insufficiency | GFR about 20 - 50% normal. Azotemia, anemia and HTN appear, get isothenuria i.e. polyuria that is almost isotonic with plasma |
| Renal Failure | GFR is 20 - 25% normal. edema, metabolic acidosis and hypercalcemia develop. May get uremia |
| ESRD | GFR < 5% normal, anuria |
b. treatment for ESRD
1. peritoneal dialysis
2. hemodialysis
3. transplantation