Kidney and Genitourinary Disorders

Kidney and Genitourinary Disorders

General Renal Principles

  • Kidney function is indicated by the glomerular filtration rate (GFR).

  • The kidneys of children reach adult GFR at approximately 1 year of age, but measured GFR vary by age.

  • GFR can be estimated (eGFR) with the patient height, serum creatinine, and a constant (Schwartz equation). eGFR mL/minute/1.73 m2 = (k)(height)/serum creatinine

    • k = constant of 0.413 for all ages/genders.

    • Height is measured in centimeters.

    • Serum creatinine is measured in mg/dL.

    • Renal blood flow is dependent on intravascular volume and adequate cardiac output with oxygenated blood.

  • Fractional excretion of sodium.

    • Equation used to determine whether kidney dysfunction is only a result of hypoperfusion to kidney.

    • Results.

      • <1% prerenal (e.g., hypovolemia, sepsis, congestive heart failure).

      • >1% intrinsic (e.g., acute tubular necrosis, glomerulone-phritis [GN]).

      • >4% postrenal (e.g., obstruction, urolithiasis).

  • BUN-to-creatinine ratio.

    • Normal ratio is 10:1 to 20:1.

    • Elevated ratios are often associated with shock or dehydration with acute kidney failure. Also may result from nephrolithiasis or gastrointestinal or pulmonary hemorrhage.

    • Low ratios are often associated with rhabdomyolysis, syndrome of inappropriate antidiuretic hormone secretion, lung disease, malignancy, low dietary protein intake, or certain medications.

Acute Renal Failure

Andrea M. Kline-Tilford


  • Many etiologies, including hemolytic uremic syndrome (HUS), shock, and GN.

  • Classified as prerenal, intrinsic renal, and postrenal.

  • Prerenal is the most common.

  • Highest mortality rates are associated with multiorgan system failure; however, complete recovery of kidney function occurs in some patients.


  • Medication history (e.g., nephrotoxic agents).

  • Vital signs (e.g., blood pressure, heart rate, temperature).

  • Fluid balance: urine output.

  • Serum electrolytes and complete blood count (CBC).

  • Consider hepatic panel if concern for hepatorenal syndrome.

  • Chest radiography if accompanied by respiratory symptoms.


  • Fluid management: judicious (e.g., restore intravascular volume or diuresis depending on clinical status). Aggressive hydration may result in fluid overload, pulmonary edema, and respiratory compromise.

  • Calculation of fractional excretion of sodium may help guide fluid management.

  • Fluid management with urine output replacement and calculated insensible losses may be warranted.

  • Hyponatremia is common. Risk for seizure activity if serum sodium <125 mEq/L. Treat with hypertonic saline solution (e.g., 3% saline administration).

  • Hyperkalemia may be life-threatening (e.g., ventricular tachycardia, ventricular fibrillation).

    • EKG findings in hyperkalemia may include peaked T waves, prolongation of PR interval, widening of QRS complex, flattening of P waves.

    • Imperative to reduce extracellular potassium level and stabilize the cardiac cell membrane to avoid ventricular tachycardia/fibrillation. Glucose, sodium bicarbonate, insulin, and albuterol shift potassium into the cells.

    • Calcium chloride can stabilize the cardiac cell membrane.

    • Sodium polystyrene can exchange potassium and sodium in the colon.

    • Emergent dialysis is often indicated for serum potassium levels >7 mEq/L.

  • Hypertension therapy: avoid angiotensin-converting enzyme (ACE) inhibitors. Goal is normal blood pressure for gender and height.

  • Adjust medications that are renally excreted; consult a pharmacist.

  • Renal supportive therapies may be indicated. See more information on renal supportive therapies later in this section.

Urinary Tract Infection

Andrea M. Kline-Tilford


  • Accounts for as many as 5% to 14% of all pediatric emergency department (ED) visits.

  • Common cause of hospitalization for infants and young children.

  • Uncircumcised males have the highest incidence in the first 3 months of life.

  • Genetic predisposition and history of dysfunctional voiding or elimination (e.g., encopresis) are associated with higher rates of UTI.

  • In otherwise healthy children, UTI may indicate an underlying abnormality in the urinary tract (e.g., vesicoureteral reflux (VUR) disease; varying degrees of severity).


  • Most common etiology is colonic organisms.

  • Commonly associated with gram-negative bacteria (e.g., Escherichia coli, Klebsiella species, and Pseudomonas aeruginosa), gram-positive bacteria (e.g., Enterococcus, Staphylococcus aureus, group B streptococcus).

  • Has also been associated with Candida, adenovirus, and herpes simplex virus.

Clinical Presentation

  • Infants/Young children: fever, irritability/fussiness, decreased appetite, lethargy or changes in activity level, jaundice, and/or weight loss.

  • Preschool/Young school age: abdominal pain, nausea/vomiting, and urinary frequency.

  • Older children: urinary frequency, dysuria, urgency, suprapubic pain, and/or nausea/vomiting.


  • Evaluate history for UTIs, structural abnormalities of the urinary tract, bubble baths, voiding/elimination dysfunction, sexual activity, maltreatment risk.

  • Physical examination: evaluate for sacral dimple, costovertebral angle, or suprapubic tenderness.

  • Urinalysis: presence of leukocyte esterase, nitrites, >5 white blood cells (WBCs), or bacteria/hpf.

  • Urine culture: identifies pathogen and evaluates antibiotic sensitivity/resistance.

    • More than 50,000 colony-forming units/mL of a single organism and pyuria represent UTI in appropriately obtained specimens.

    • Must consider collection method/route and clinical presentation.

    • Urinalysis and urine culture are recommended to determine the presence of a UTI.

  • Imaging.

    • Ultrasound: evaluates anatomy, kidney size/shape, and for evidence of hydronephrosis. Can also be used to evaluate for areas of inflammation and signs of pyelonephritis. Indications: UTI in children 2 months to 2 years of age.

    • Voiding cystourethrography: If renal and bladder ultrasound show hydronephrosis, scarring, or other evidence of high-grade VUR or obstructive uropathy, as well as in other atypical or complex clinical circumstances. Also indicated in all infants 2 months of age to 2 years with recurrence of febrile UTI.

    • Dimercaptosuccinic acid (DMSA) scintigraphy: Nuclear medicine scan used to evaluate for renal scarring.


  • Antibiotic therapy, tailored to specific organism when culture and sensitivities are available.

    • Duration of therapy determined by patient age, severity of illness, local resistance patterns, associated underlying disorders.

    • Uncomplicated UTI duration of therapy is 7 to 10 days; some studies support shorter duration of 2 to 4 days of therapy.

    • Complicated UTI therapy is generally 14 days.

    • Trimethoprim-sulfamethoxazole, amoxicillin-clavulanate, cefixime are acceptable selections for initial oral therapy.

    • Ceftriaxone, cefotaxime, gentamicin are acceptable selections for initial parenteral therapy.

    • In general, oral antibiotics are equally effective as parenteral therapy.

  • Discomfort/fever: acetaminophen.

  • Hospitalization is recommended when children are unable to tolerate oral medications or maintain adequate hydration, failure to improve on outpatient therapy, evidence of sepsis/septic shock, or underlying medical conditions that may complicate the management of UTI.

  • Patient family education: signs of UTI, hygiene, limiting bubble baths, constipation prevention, urination after intercourse if sexually active.

  • Close clinical follow-up after 7 to 10 days of antimicrobial therapy to evaluate for recurrent UTI.


Samantha Lee

Most Common Etiologies

  • Gram-positive bacteria: Enterococcus spp. and Staph. aureus.

  • Gram-negative bacteria: E. coli, Klebsiella spp., Proteus spp., P. aeruginosa, Serratia spp., and Enterobacter aerogenes.


  • 60% to 65% of children with febrile UTI also have acute pyelonephritis.

  • Most cases of acute pyelonephritis respond readily to antibiotics.

Clinical Presentation

  • Fever, lethargy.

  • Tachycardia, tachypnea, dehydration.

  • Pain (abdominal, suprapubic, flank, and/or costovertebral).

  • Odorous urine.

Diagnostic Evaluation

  • Urinalysis: rapid detection of leukocyte esterase and nitrites.

  • Urine culture with sensitivities: critical for determining organism and appropriate antibiotic therapy.

  • Basic metabolic panel: evaluation of kidney function.

  • CBC with differential: evaluation of WBC count and differential.

  • Blood culture: Positive culture indicates bacteremia.

  • C-reactive protein: elevated, indicating an inflammatory process.

  • Erythrocyte sedimentation rate: elevated, indicating an inflammatory process.

  • Renal ultrasound for children 2 to 24 months of age.


  • Intravenous (IV) antimicrobial therapy.

  • Hydration.

  • Renal ultrasound.

  • Voiding cystourethrography (VCUG): in some cases.

    • VCUG is typically reserved for children with recurrent febrile UTI who have evidence of abnormalities on ultrasound.


Samantha Lee


  • Primary (acute poststreptococcal GN, most common form) (see next section).

  • Secondary.

  • Hereditary.

Clinical Presentation

  • History of recent throat infection, decreased urine output, dark urine, fatigue, headache.

  • Rash on buttocks and posterior legs, arthralgia, and weight loss (symptoms of secondary GN).

  • Elevated blood pressure.

  • Edema.

  • Other signs of fluid overload/congestive heart failure.

Diagnostic Evaluation

  • Electrolyte panel, creatinine, BUN, CBC with differential, urinalysis with urine culture and sensitivities, and throat culture.

  • If acute poststreptococcal GN is suspected, a serum antistreptolysin-O (ASO) titer should be checked.

  • To assess for systemic disease, autoimmune panels such as serum complement levels (C3, C4), lupus serologies, anti-DNase B, perinuclear antineutrophil antibody (P-ANCA), cellular antineutrophil cytoplasmic antibody (C-ANCA), and IgA are useful.

  • Low serum C3 levels are indicative of secondary GN.


  • Antibiotic: penicillin, first line.

  • Treatment of hypertension or acute renal insufficiency.

    • Judicious fluid management.

    • Sodium-restricted diet.

    • Diuretics.

    • Calcium channel antagonists, vasodilators, or ACE inhibitors.

  • For secondary forms of GN.

    • Corticosteroids and cyclophosphamide to counteract the inflammatory process.

Acute Poststreptococcal Glomerulonephritis

Tamara L. Hill


  • Commonly follows group A streptococcal pharyngitis during the cold weather months and streptococcal skin infections or pyoderma during warm weather months.

Clinical Presentation

  • Sudden onset of gross hematuria, edema, hypertension, and renal insufficiency.

Diagnostic Evaluation

  • Urinalysis: red blood cells—often associated with red blood cell casts, proteinuria, and polymorphonuclear leukocytes.

  • Elevated ASO titer.

  • Complement level: C3 level initially decreased; returns to normal 6 to 8 weeks after presentation (sometimes sooner).

  • Throat culture positive for group A streptococcus can confirm diagnosis.


  • Penicillin: a 10-day course.

  • Cephalosporins or macrolide antibiotics can be used in patients with penicillin allergy.

  • Acute renal insufficiency: furosemide.

  • Hypertension: antihypertensive agents and sodium restriction.

Renal Artery/Vein Thrombosis

Samantha Lee

Andrea M. Kline-Tilford


  • Relatively rare.

  • Most commonly associated with asphyxia, sepsis, shock, dehydration, hypercoagulable state, indwelling umbilical catheter, or maternal diabetes in newborns/infants.

  • Also associated with nephrotic syndrome, congenital heart disease, inherited hypercoagulable state (e.g., Factor V Leiden deficiency), sepsis, exposure to contrast agents, or after kidney transplantation in children.

Clinical Presentation

  • Abrupt onset of hematuria.

  • Flank mass, unilateral or bilateral.

  • Flank pain.

  • Oliguria.

  • Hypertension.

Diagnostic Evaluation

  • Doppler ultrasound of kidneys is diagnostic.

  • Ultrasound: enlarged kidney(s) (early stages), atrophic kidney(s) (late stages).

  • Radionuclide study: minimal or no function in the affected kidney(s).

  • Abdominal CT: filling defect during venous phase after contrast administration.

  • Magnetic resonance venography may also be used; avoid administration of contrast.

  • Microangiopathic hemolytic anemia; thrombocytopenia in some cases.


  • Monitor and maintain fluid and electrolyte balance.

  • Blood pressure monitoring; antihypertensive agents.

  • If refractory to pharmacologic therapy, may require nephrectomy.

  • Treatment with anticoagulants (e.g., heparin) or thrombolytics (e.g., streptokinase, recombinant tissue plasminogen activator) is common, but controversial.

  • Inferior vena cava thrombus may require thrombectomy.

  • Treat underlying disease (e.g., nephrotic syndrome), if indicated.

Renal Tubular Acidosis

Samantha Lee


  • Result of an inherited or acquired defect that affects the kidneys’ ability to filter bicarbonate or excrete ammonia.

  • Sickle cell anemia can be a genetic cause of renal tubular acidosis (RTA).

  • Acquired causes: certain medications, obstructive uropathy, and autoimmune diseases.

  • Often associated with presence of a UTI.


  • Type I RTA (distal): decrease in acid excretion.

  • Type II RTA (proximal): failure of bicarbonate reabsorption with decreased ammonium absorption.

  • Type IV RTA: aldosterone deficiency or impairment of its effects, resulting in reduced potassium excretion, hyperkalemia, and acidosis.

  • Types I and II are most common in children.

Clinical Presentation

  • Polyuria.

  • Polydipsia.

  • Preference of savory foods.

  • Hypokalemia.

  • Refractory rickets.

  • Metabolic acidosis.

Presentation of Specific Types

  • Type I RTA: linked to multiple genetic disorders (sensorineural hearing loss and nephrocalcinosis); failure to thrive or short stature, anorexia, vomiting, and dehydration.

  • Type II RTA: failure to thrive, hyperchloremic acidosis with hypokalemia, and rarely nephrocalcinosis; rickets or osteomalacia may indicate Fanconi syndrome.

  • Type III RTA: no longer used as a classification; now thought to be a combination of types I and II.

  • Type IV RTA: Hypertension common if child has underlying Gordon syndrome, renal parenchymal disease, or mineralocorticoid dysfunction.

Diagnostic Evaluation

  • Serum and urine electrolytes.

  • Fractional excretion of bicarbonate and urine pH.

  • Urine glucose and protein, calcium-to-creatinine ratio.

  • 24-hour urine sample (i.e., citrate, calcium, potassium, and oxalate).

  • Radiographies of long bone or wrists for evaluation of rickets.

  • Abdominal ultrasound (kidneys).

  • Genetic or chromosomal evaluation.


  • Emergency or impatient management for children with hyperchloremic, non-anion gap acidosis requiring bicarbonate replacement intravenously.

  • Slow rehydration and electrolyte replacement, sodium bicarbonate or citrate, diuretic, phosphate replacements in children with rickets.

Hemolytic Uremic Syndrome

Tamara L. Hill


  • Divided into Shiga-toxin-associated HUS and non-Shiga-toxin-associated HUS based on clinical presentation.

  • Shiga-toxin-associated HUS occurs after a prodromal episode of bloody diarrhea caused by E. coli infection.

  • Non-Shiga-toxin-associated HUS is distinguished by absence of diarrhea or Shiga-toxin-producing E. coli infection, but with microangiopathic hemolytic anemia, thrombocytopenia, and uremia.

Clinical Presentation

  • Gastroenteritis with fever, vomiting, diarrhea, abdominal pain, and diarrhea that begins as watery but then becomes bloody.

  • Physical examination: dehydration, edema, petechiae, hepatosplenomegaly, and marked irritability.

Diagnostic Evaluation

  • Hemoglobin level is commonly 5 to 9 g/dL.

  • Peripheral blood smear reveals helmet cells, burr cells, and fragmented red blood cells.

  • Reticulocyte count is moderately elevated.

  • Coombs test result is negative.

  • Significant leukocytosis with the leukocyte count greater than 300,000/mm3.


  • Supportive care.

  • Aggressive management of fluids, electrolytes, and nutrition.

  • Control of hypertension and early initiation of dialysis have been associated with a decrease in mortality.

Nephrotic Syndrome

Tamara L. Hill

Samantha Lee


  • Idiopathic (90%).

  • Believed to have immunopathogenesis.

  • Genetic disorders.

  • Secondary causes include infection, drugs, immunologic/allergic disorders, association with malignant disease, glomerular filtration.

Clinical Presentation

  • Edema: most notably, periorbital edema.

  • Frothy or foamy urine.

  • Sudden increase in weight with edema.

  • Hypertension.

  • Hypoalbuminemia.

  • Hyperlipidemia.

Diagnostic Evaluation

  • Urine dipstick to determine proteinuria (rapid).

  • 24-hour urine collection (ideal).

  • CBC with differential.

  • Complete metabolic panel with serum albumin.

  • Serum C3/C4 complement.

  • Antinuclear antibody.

  • Hepatitis B and C.

  • HIV testing.

  • Immunologic studies (IgG, IgM, IgE).

  • Kidney biopsy.


  • High-dose steroids (prednisone 2 mg/kg/day for 6 weeks divided into three doses).

  • Treatment continues until patient is in remission (3 days with zero-trace protein via urine dipstick).

  • Once proteinuria is resolved, maintenance dose of steroids—2 mg/kg every other morning, then tapered off over 6 weeks.

  • If no remission after initial treatment, patient is considered steroid-resistant. Begin cytotoxic medications such as cyclosporine A, cyclophosphamide, or chlorambucil.

  • Supportive therapy includes ACE inhibitors, statins, and diuretics, and restricting dietary sodium to 1,500 to 2,000 mg/day.

Henoch-Schönlein Purpura Nephritis

Tamara L. Hill

Clinical Presentation

  • Symptoms usually present 1 to 3 weeks after an upper respiratory tract infection or gastrointestinal infection (e.g., Epstein-Barr virus, parvovirus B19, Helicobacter pylori infection, Yersinia infection, Shigella infection, Salmonella infection), or environmental allergen exposure (e.g., medications, foods, insect bites).

  • Raised, nonblanching, purpuric rash, most prominent on the buttocks and lower legs.

  • Abdominal pain.

  • Arthralgias.

  • GN.

  • Presentation may be acute or insidious.

Diagnostic Evaluation

  • Clinical presentation.

  • Gross hematuria.

  • Urinalysis: microscopic or gross hematuria and proteinuria.

  • CBC: leukocytosis with eosinophilia, thrombocytosis.

  • D-dimer: increased.

  • Prothrombin time and activate partial thromboplastin time: decreased.

  • IgA levels: may be increased.

  • Stool guaiac test: occult blood.

  • Kidney biopsy findings are indistinguishable from those of IgA nephropathy.


Jan 30, 2021 | Posted by in NURSING | Comments Off on Kidney and Genitourinary Disorders

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