Upper Urinary Tract Disorders

4. Vesicourethral reflux (VUR)
1. Definition: retrograde flow of bladder urine into the ureters
2. Etiology
1. primary (congenital anomaly)
2. secondary (acquired, usually associated with UTI)
3. Pathophysiology
1. bladder reflux
2. residual urine from ureters remains in bladder until next void
3. increases chance for and perpetuates infection
4. vesicoureteral reflux grading system: grade one to five
4. Findings: UTI with chronic findings & recurrences
5. Diagnostics: radiographic studies
6. Management
1. medications: for grades one to four, low-dose antibiotics; monitor
2. surgery: for severe cases, grade four or grade five
7. Concerns:
1. renal scarring
2. all children in family should be screened
   
5. Acute glomerulonephritis (AGN)
1. Etiology
1. acute bacterial infection (pharyngitis, impetigo)
2. underlying systemic disorder
2. Pathophysiology
1. infection (usually group A B-Hemolytic strep) provokes immune complex response
2. immune complexes trapped in glomerular capillary loop
3. activate inflammatory response, which injures capillary walls
4. decrease lumen functions and GFR (glomerular filtration rate)
5. decreased filtration of plasma results in excessive acummulation of water and retention of sodium
6. onset appears after latent period of about ten days
   
3. Findings
1. oliguria
2. edema (periorbital and peripheral)
3. hematuria ("smoky" or "tea-colored" urine)
4. mild hypertension
5. lethargy
6. moderate proteinuria
7. loss of appetite
4. Diagnostics: urine testing, serum (antibody, complement, CRP, ESR, WBC), throat culture, history of antecedent strep infection
5. Management
1. no specific treatments; recovery spontanteous and uneventful in most cases
2. supportive with careful regulation of fluid balance; I & O, daily weights
3. medications: antihypertensives, if needed
4. possible diuretic nutrition (low in sodium, protein, potassium)
6. Concerns: hypertensive encephalopathy, cardiac decompensation, renal failure, edema and fluid overload
   
6. Chronic nephrosis = nephrotic syndrome
1. Massive proteinuria, hypoalbuminemia, hyperlipemia and edema
2. Etiology: not fully understood - possibly renal lesions or other processes
1. types:
1. primary (idiopathicnephrosis): restricted to glomerular injury
2. secondary: develops as part of systemic illness
3. Pathophysiology
1. glomerular alteration and increased permeability to plasmaproteins, especially albumin
2. plasma protein losses; increased presence in urine, decrease plasma volume, colloidal osmotic pressure in capillaries decreases
3. hydrostatic pressure is greater than colloidal osmotic pressure resulting in fluid accumulation in interstitial spaces and body cavities
4. shift in plasma fluid leads to hypovolemia
5. hypovolemia - triggers kidneys to produce renin, and angiotensin which stimulates the release of aldosterone and increases the reabsorbtion of water and sodium
6. aldosterone increases
7. decreased blood pressure also causes release of ADH leading to increase in water absorption
4. Findings
1. progressive weight gain
2. puffiness of face
3. generalized edema (insidious)
4. periorbital edema
5. loss of appetite
6. oliguria
7. lethargy
8. pallor
5. Diagnostics: history, urine tests: massive proteinuria, serum testing
6. Management: mainly supportive
1. diet: limit sodium, but high potassium and protein
2. medications: corticosteroids, immunosuppressants, diuretics
7. Concerns: hypercoagulability and thrombosis, fluid excess, alterations in skin integrity, recurrence
   
7. Hemolytic uremic syndrome (HUS)
1. Definition
1. acute disorder shows the "triad":
1. hemolytic anemia
2. thrombocytopenia
3. acute renal failure
2. occurs most often in children under four
2. Etiology: unknown; some association with genetics, endotoxins, bacteria (E. coli, rickettsia, coxsackie), enzyme deficiency, decreased antioxidants
3. Pathophysiology
1. usually follows an acute GI or upper respiratory infection (URI)
2. pathogen attaches to GU tract
3. GU tract produces toxins that damage capillary walls
4. inflammation - glomerular vessels less capable of filtration
5. anemia occurs (due to RBC fragmentation)
6. thrombocytopenia (due to platelets trapped in small vessels)
4. Findings
1. prior URI
2. rapid onset of pallor
3. accompanying hemorrhagic manifestations such as bruising or rectal bleeding
4. triad
5. hypertension
5. Diagnostics: identify "triad" from history and lab testing
6. Management
1. supportive
2. for anemia: transfusions
3. for renal symptoms: fluids, possible dialysis
4. treatment of hypertension
5. correction of acidosis and electrolyte disorders
6. concern: renal impairment