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





Etiology



  • 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.


Evaluation



  • 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.


Management



  • 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



Background



  • 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).


Etiology



  • 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.


Evaluation



  • 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.


Management



  • 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.



Pyelonephritis

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.


Background



  • 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.


Management



  • 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.


Nephritis

Samantha Lee



Etiology/Types



  • 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.


Management



  • 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



Etiology/Types



  • 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.


Management



  • 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



Background



  • 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.


Management



  • 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


Background



  • 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.




Etiology/Types



  • 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.



Management



  • 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



Etiology



  • 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.


Management



  • 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



Etiology



  • 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.


Management



  • 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.


Management

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