↑↓ renal

UTI:

lower: urethra and bladder (urethritis/cystitis)

upper: ureters, renal pelvis, calyces, and renal parenchyma

dx. urine dipstick — presence of leukocytes, esterase and nitrites, bacteria and WBC

• Culture and sensitivity-clean catch or catherization

• Bacteria colony count is >50,000/ml

trx. antibiotics (Trimethoprim-sulfamethoxazole (TMP-SMX)…)

• analgesics/antipyretics

prevention: Perineal hygiene—wipe from front to back.

• Avoid tight clothing or diapers;

• wear cotton Underwear rather than nylon.

• Avoid “holding” urine stasis

• Encourage generous fluid intake

• Prevent constipation

• urinate after intercourse

voiding cystourethrography

contrast injected into bladder until full and takes pictures before, during, and after to visulize bladder outline and urethra revealing reflux of urine into ureters and abnormalites of bladder emptying

vesicoureteral reflux (VUR)

urine backflows from bladder → upper urinary tract

Primary reflux: congenital anomaly that affects the ureterovesical junction.

Secondary reflux: anatomic or functional bladder obstruction → abnormally high pressure in the bladder

•Renal scarring predisposes to kidney disease

s/s. UTI s/s

dx. culture

trx. Continuous antibiotic prophylaxis (CAP)

• Surgery or Endoscopy

  • Breakthrough febrile UTIs despite antibiotic prophylaxis

  • Severe reflux

  • Mild or mod reflux in females persists puberty

  • Poor compliance with medications or surveillance

  • Poor renal function or appearance of new scars

• Screen siblings-Renal ultrasound

Acute Glomerulonephritis (AGN)

Immune complex formation and glomerular deposition → ↓ GFR → ↑ retention of water and Na → edema and HTN

Types:

1. Post Infection (Pneumococcal, streptococcal, or viral)

2. Primary

3. Systemic Disorder Manifestation (SLE, SCD, Bacterial endocarditis)

s/s: Low C3 complement levels

• Periorbital, lower extremity edema

• Loss of appetite

• ↓ u/o -oliguria

• Cola colored urine

trx. Bed rest acute phase

• B/P every 4 to 6 hours; Seizure precautions

Diet: Na and h2o restrictions, Potassium and protein restricted with oliguria

• Antibiotic therapy-strep positive

•1st sign of improvement= increased urine output

•Decrease in body weight (edema decreases)

•BP returns to normal

•Hematuria and proteinuria may persist for months to years

•Renal function typically returns to normal by 8 wks

chronic glomerulonephritis

Tissue damage and progression to fibrosis → change glomerular structure → end-stage renal disease (ESRD)

dx. ↑ BUN, creatinine, and uric acid levels

s/s. Hypertension, edema, intermittent gross hematuria

• Metabolic acidosis, ↑ potassium, and ↓ calcium levels

trx. Prolonged course

• Corticosteroids or cytotoxic agents, Antihypertensive, erythropoietin and iron

• Dialysis/Transplant for end stage

Nephrotic syndrome

Glomerular injury causing permeability to plasma protein → Massive urinary protein loss and Edema

3 Types:

1. Minimal Change Nephrotic Syndrome (MCNS)- Most common primary

2. Secondary Nephrotic Syndrome (SNS)

• where the disease is caused by systemic conditions such as AGN & CGN most common

3. Congenital Nephrotic Syndrome-Finnish Type (CNS)

•Autosomal recessive disorder manifesting w/in 1^st months of life → Death before 3 yrs w/o treatment

s/s. Generalized edema (anasarca)

• Pitting edema, Weight gain, Ascites, abdominal pain

• Pallor, fatigue,

• Decreased u/o

tx. Diet: ↓ protein, ↓ Sodium,

Prednisone: 2 mg/kg divided into BID doses

• u/o will start to increase within  7 to 21 days of therapy

Immunosuppressant therapy (Cytoxan)

Diuretics

nursing consideration:

• I&O’sDaily weights

•Physical assessment including severity of edema

•Ascites: Measurement of abd girth

•Nutritional education

•Medication compliance

•Psycho-social considerations