peds endocrine and renal

• Pyelonephritis

  Urinary tract infection is inflammation of the bladder and or the kidney almost always caused by bacteria that move up the urethra and into the bladder causing bladder infection
• Pyelonephritis

  1. Bacteria goes up kidneys

  2. Severe pyelonephritis primary cause of renal scarring- HTN, chronic kidney disease
• UTIs

  • Significant number of organisms anywhere in the urinary tract
  • Difficult to localize the infection
  • Common in early childhood
  • Common in female due to shorter urethra
• UTI Treatment

  1. Goals: Treat infection, determine if anatomical variation contributes, Preserve renal function, Prevent systemic infections

  2. Preventative measures- hygiene

  3. Antibiotics determined by identification of organism: penicillins, sulfonamide, cephalosporin, nitrofurantoin

  4. Surgical correction of anatomical abnormalities

  5. Education on medication and preventive measures
• Contributing Factors to UTIs

  • Stasis – urine that is not excreted frequently and completely allows overgrowth
  • Low fluid intake
  • Alkaline pH
  • Reflux can lead to incomplete bladder emptying
• Causative Organisms for UTIs

  • E Coli (80%)
  • Proteus
  • Pseudomonas
  • Klebsiella
  • Enterobacter
  • Enterococcus
  • Staphylococcus
  • Haemophilus
• Clinical Presentation of UTIs

  • Neonate: poor feeding, respiratory distress, temp instability-febrile, jaundice
  • Infant- 2yrs: poor feeding, diarrhea, crying on urination, frequency, foul smelling, enlarged kidneys or bladder, diaper rash, seizures, fever, irritability, lethargy
  • Older child: enuresis, daytime incontinence, fever, foul smelling urine, frequency/urgency, may also complain of abd pain, flank pain, hematuria, vomiting, pain w urination
• Diagnostic Tests for UTIs


  • Urine collection methods
  • IVP- intravenous pyelogram- xray that uses an injection of contrast material to evaluate kidneys, uterus, and bladder
  • Voiding Cystourethrogram- exam that takes images of urinary system. Bladder is filled w contrast material then images of bladder and kidneys taken as the bladder fills and while the pt urinates
  • Ultrasound
  • Renal scan
  • Cystoscopy
• Vesicoureteral Reflux (VUR)

  • Normal Ureters valves close to prevent retrograde reflux
  • In VUR, valves fail to close. (May be related to depth of implantation in the bladder wall)
  • Retrograde flow of urine from the bladder back into the kidneys creating a reservoir for bacteria and may cause pyelonephritis
  • Severe pyelonephritis is the primary cause of acquired renal scarring in childhood, which may eventually lead to hypertension and chronic kidney disease in a small fraction of patients
• Grades of VUR

  • I- reflux to the ureter only
  • II-reflux into the ureter & renal pelvis without distention
  • III-reflux into the ureter & renal pelvis causing mild hydronephrosis
  • IV-moderate hydronephrosis
  • V – severe hydronephrosis & twisting of the ureters
• VUR Treatment

  1. Wait to see if they will outgrow- high-rate spontaneous resolution (especially grade 1&2)

  2. Antibiotic prophylaxis (trimethoprim, sulfamethoxazole, nitrofurantoin)

  3. Culture urine fever/symptomatic

  4. May stop antibiotics once toilet trained or asymptomatic

  5. Significant anatomical abnormalities require surgical correction

  6. Surgical correction (mostly laparoscopic) depending on extent of repair needed

  7. Reimplantation of the ureters

  8. Obstruction correction

  9. Dilatation – urethra
• Nursing Care for VUR

  1. Conservative-

  2. Assure abx compliance and follow-up

  3. Surgical-

  4. Foley/Suprapubic Catheter maintenance – free flow, no clots

  5. Pain management

  6. Morphine, fentanyl, ketorolac

  7. Antispasmodics – oxybutynin

  8. Hydration – will be 1.5-2 X maintenance

  9. Wound management if present
• Hydronephrosis

  Dilatation of the renal pelvis due to an obstruction (kidney stone, scarring, congenital malformation, ect) of urine flow in or out of the bladder
• Common features of Acute Glomerulonephritis

  • Oliguria
  • Edema
  • Hypertension
  • Circulatory congestion
  • Hematuria
  • Proteinuria
• Causes of Acute Glomerulonephritis

  • Many cases post infection
  • Streptococcal
  • Pneumococcal
  • Viral infections
  • Systemic Disease Process
  • Systemic lupus erythematous
  • Sickle cell disease
• Acute POST streptococcal glomerulonephritis (APSGN)

  • Most common in school age kids
  • Reaction following preceding strep infection
  • Current theory – membrane shed into circulation triggers antibodies, immune-complex reaction occurs
  • Edema & cell proliferation alters loop structure & function. This leads to excessive accumulation H2O & retention Na (expanded fluid volume, circulatory congestion, edema, hypertension)
• Signs and Symptoms of APSGN

  • Symptoms persist about 4-10 days (Can be 2-3 weeks)
  • Facial edema, especially periorbital
  • Tea/cola colored urine
  • Oliguria
  • Anorexia
  • Elevation in B/P
  • Irritable, lethargic
  • First sign of improvement is an increase in urine output
  • Hematuria improves and Creatinine and BUN gradually return to normal
  • Moderate proteinuria may persist several weeks
• Complications of APSGN

  • Hypertensive Encephalopathy – autonomic regulatory mechanisms fail ® hyper perfusion of the CNS leads to Cerebral edema
  • Decreased LOC
  • Seizures
  • Headache, dizziness, vomiting
  • Cardiac Decompensation – hypervolemic stage
  • enlarged heart
  • pulmonary edema
  • Acute kidney injury
• Diagnosis of APSGN

  • Streptococcal antibody titers
  • Urinalysis
  • Hematuria
  • Proteinuria (mild)
  • Increased specific gravity
  • Pharynx culture- if positive for bacteria, antibiotic treatment
  • Azotemia (Increased serum BUN & creatinine)
  • Chest x-ray – Circulatory overload can lead to respiratory distress
• Treatment of APSGN


  1. Recovery usually spontaneous without complications

  2. General – supportive care & early identification of complications

  3. Careful monitoring whether treatment home or hospital

  4. Edema - daily weight, I & O, may restrict water and Na intake

  5. diuretics –limited value May be used if renal failure not severe

  6. If Hypertension – B/P, antihypertensives

  7. If concerns for Seizures – anticonvulsants

  8. Diet – if renal failure present – may restrict protein, K & Na. If not severe – normal diet with no added salt

  9. Antibiotics used only for persistent infections
• Nursing Considerations for APSGN

  1. Careful assessment & monitoring

  2. VS- BP every 4-6 hours

  3. Daily weight

  4. Fluid status

  5. Volume & characteristics of urine

  6. General appearance

  7. Behavior

  8. If fluid restriction, plan how to distribute allowed fluid over waking hours

  9. Educating patient and family, monitoring follow-ups
• Chronic Glomerulonephritis

  • Progressive renal disease with tissue damage r/t immune response & inflammation
  • May have prolonged course and poor prognosis
  • May have minimal signs early, often more common adolescents when symptomatic
  • Diagnosis - Renal Biopsy
  • May have some response to cytotoxic agents or glucocorticoids
  • Antihypertensives
  • Some rapid deterioration, ESRD
  • Dialysis/ Renal transplant
• Nephrotic Syndrome

  • Increased glomerular permeability which allows massive loss of protein through urine
  • Massive proteinuria, hypoalbuminemia, hyperlipidemia, edema
• Forms of Nephrotic Syndrome

  • Minimal Change Nephrotic Syndrome- most common. Usually seen preschool age. Often preceded by viral upper respiratory infection. Thought to be precipitating, not cause
  • Secondary- often caused by AGN or CGN. Can be related to collagen vascular disease like disseminated lupus or drug toxicity, stings or venom
  • Congenital- recessive gene. Symptoms early infancy. Can lead to death if not adequate treatment
• Minimal Change Nephrotic Syndrome

  • Disturbance in the basement membrane of the glomeruli causes increased permeability, specifically protein
  • Decrease in colloid oncotic pressure (A form of osmotic pressure induced by proteins) which causes a leakage of fluids from the capillaries
  • Massive proteinuria (albumin), hypoalbuminemia, hyperlipidemia
  • Increase 3rd space fluid- edema, especially abdominal cavity
  • Loss of vascular volume
  • Sodium & H2O reabsorption to increase vascular volume
• Signs and Symptoms of Nephrotic Syndrome

  • Weight gain- facial puffiness morning, edema abdomen, genitalia, lower extremities more prominent over day
  • Generalized edema
  • Intestinal edema may cause diarrhea, poor appetite
  • Microscopic or absent hematuria
  • Severe proteinuria
  • Low serum protein
  • Normal or slightly decreased blood pressure
  • At risk for infection
  • Skin breakdown r/t edema
• Diagnosis of Nephrotic Syndrome

  • History and clinical presentation
  • Urinalysis
  • Protein
  • Increased specific gravity
  • Serum
  • Decreased protein concentrations- hypoabluminemia
  • H&H norm to elevated, Platelets elevated
  • Hyponatremic
  • Ion Calcium used for better measure of calcium levels as Total Calcium low since binds to albumin
  • Hypercholesterolemia
  • Renal Biopsy
• Treatment of Nephrotic Syndrome

  1. Objective: to reduce excretion of protein

  2. Primarily supportive treatment

  3. Corticosteroids daily for 4-6 weeks then weaning schedule 2-5 months (Prednisone steroid of choice)

  4. Response usually within 7-21 days

  5. Diet - if no renal failure - encourage protein, no restriction on water. No added salt

  6. Monitor for Skin issues

  7. I & O, abdominal girth

  8. Protect from infection

  9. Diuretics have limited effectiveness. May be used with extreme edema

  10. Relapses 1-3 x/year (risk of frequent steroid use)

  11. Immunosuppressant therapy reduces relapse rate and increases remission time. Cyclophosphamide, Cyclosporine or Mycophenolate

  12. Rituximab when steroid resistant with frequent relapse

  13. Awareness of complications from immunosuppressants important
• Side Effects of Nephrotic Syndrome Medications

  • Cyclophosphamide
  • Bone marrow depression
  • Neutropenia
  • Gonadal toxicity
  • Hemorrhagic cystitis – damage to the bladder which can result in hematuria and dysuria
  • Cyclosporine or mycophenolate mofetil
  • Nephrotoxicity
  • Increased risk infections
• Nursing Considerations for Nephrotic Syndrome

  1. Careful monitoring I&O

  2. Daily weight

  3. Abdominal girth

  4. Urine for albumin

  5. Assessment edema, skin integrity

  6. Small frequent meals to promote nutrition

  7. Salt, fluid restriction with edema

  8. Family education to recognize symptoms of relapse. Urine testing for albumin. Med management
• Hemolytic Uremic Syndrome (HUS)

  • Most often associated with enteric pathogens (E Coli) in the US. As these pathogens are broken down in the body they release toxins which can effect vasculature, platelets and the renal system
  • Usually in young children – 6 mo -3 years
  • Triad: Acute Kidney Injury, Hemolytic anemia, Thrombocytopenia
  • Arterioles- occlude with platelets
• Cyclophosphamide

  • Bone marrow depression
  • Neutropenia
  • Gonadal toxicity
  • Hemorrhagic cystitis – damage to the bladder which can result in hematuria and dysuria
• Cyclosporine or mycophenolate mofetil

  • Nephrotoxicity
  • Increased risk infections
• Hemolytic Uremic Syndrome (HUS)

  1. Arterioles- occlude with platelets & fibrin clots

  2. Damaged rbc's move through spleen, which removes damaged RBCs resulting in acute hemolytic anemia

  3. Platelet aggregation in arterioles or removal of damaged platelets results in thrombocytopenia
• Signs and Symptoms of Hemolytic Uremic Syndrome (HUS)

  • Early S/S – Vomiting and diarrhea
  • Hemolytic process for several days to weeks
  • Irritability, anorexia, pallor
  • Bruising, purpura, rectal bleeding
  • Often hypertensive
  • Oliguric ® anuric
  • May have signs acute heart failure
  • Seizures
• If s/s go unrecognized or untreated Hemolytic Uremic Syndrome (HUS) can lead to death
• Treatment of Hemolytic Uremic Syndrome (HUS)


  1. Diagnosis – Presence of triad of – Acute Kidney Injury, Anemia, & Thrombocytopenia

  2. Symptom support- fluid balance, tx hypertension, correction acidosis and electrolyte imbalance

  3. Hemodialysis, Peritoneal Dialysis, or Continuous venous Hemofiltration (CVVH)

  4. Plasmapheresis

  5. Fluid Balance – Calculate carefully

  6. RBC transfusion – monitor carefully

  7. Enteral feedings when vomiting/diarrhea resolve
• Hypopituitarism

  Deficiency of pituitary hormones- gonadotropin, GH, TSH, corticotropin deficiency
• Growth hormone (GH) deficiency in Hypopituitarism

  • May be moderate to severe
  • Often grow normally in the first year
  • Growth falls off in the second year when severe ¯ 3rd percentile
  • Height more affected than weight
  • Bone age is delayed
  • May have developmental implications
• Diagnosis of Hypopituitarism

  1. Family History

  2. R/O other physical causes such as tumors

  3. Skeletal survey bone age

  4. Growth Hormone Studies (stimulate GH production)

  5. Arginine

  6. Insulin – hypoglycemia increases GH secretion