Rosen & Barkin's 5-Minute Emergency Medicine Consult (482 page)

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Authors: Jeffrey J. Schaider,Adam Z. Barkin,Roger M. Barkin,Philip Shayne,Richard E. Wolfe,Stephen R. Hayden,Peter Rosen

Tags: #Medical, #Emergency Medicine

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
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Discharge Criteria

Mild cases of clinical nephritis in healthy patients with:

  • No comorbid illness
  • Strict supervision/monitoring of symptoms, diet, urine output, and medication
  • Close follow-up with PMD and nephrology referral
Issues for Referral

Nephrology:

  • Within 2–3 days
FOLLOW-UP RECOMMENDATIONS
  • Adherence to antibiotic and antihypertensive therapy, as indicated
  • Restrict salt and fluid intake.
PEARLS AND PITFALLS
  • Diagnosis is confirmed by biopsy showing characteristic crescent formation within renal glomeruli.
  • Must obtain thorough history of ongoing or recent infections as possible etiology of nephritis
  • IgA nephropathy is most common cause of nephritis.
  • Patients require aggressive management of BP and volume status.
ADDITIONAL READING
  • Ikee R, Kobayashi S, Saigusa T, et al. Impact of hypertension and hypertension-related vascular lesions in IgA nephropathy.
    Hypertens Res
    . 2006;29(1):15–22.
  • Kanjanabuch T, Kittikowit W, Eiam-Ong S. An update on acute postinfectious glomerulonephritis worldwide.
    Nat Rev Nephrol
    . 2009;5:259–269.
  • Kunz R, Friedrich C, Wolbers M, et al. Meta-analysis: Effect of monotherapy and combination therapy with inhibitors of the renin angiotensin system on proteinuria in renal disease.
    Ann Intern Med
    . 2008;148(1):30–48.
See Also (Topic, Algorithm, Electronic Media Element)
  • Acute Renal Failure
  • Glomerulonephritis
  • Nephrotic Syndrome
CODES
ICD9
  • 580.0 Acute glomerulonephritis with lesion of proliferative glomerulonephritis
  • 580.9 Acute glomerulonephritis with unspecified pathological lesion in kidney
  • 583.2 Nephritis and nephropathy, not specified as acute or chronic, with lesion of membranoproliferative glomerulonephritis
ICD10
  • N00.9 Acute nephritic syndrome with unsp morphologic changes
  • N01.9 Rapidly progr nephritic syndrome w unsp morphologic changes
  • N05.9 Unsp nephritic syndrome with unspecified morphologic changes
NEPHROTIC SYNDROME
Maureen L. Joyner
BASICS
DESCRIPTION
  • Diseases causing defect in glomerular filtration barrier, producing proteinuria:
    • Proteinuria >3 g in 24 hr
    • Hypoalbuminemia (serum albumin <3 g/dL)
    • Peripheral edema due to hypoalbuminemia
    • Hypogammaglobulinemia
    • Hyperlipidemia (fasting cholesterol >200 mg/dL)
  • Urine fat (oval fat bodies, fatty/waxy casts)
  • Glomerular basement membrane altered by:
    • Immune complexes
    • Nephrotoxic antibodies
    • Nonimmune mechanisms
    • Result: More permeable glomerular membranes and excretion of albumin and large proteins
PATHOPHYSIOLOGY
  • Proteinuria due to increased filtration within renal glomeruli
  • Edema due to sodium retention and hypoalbuminemia
  • Postural hypotension, syncope, and shock due to severe hypoalbuminemia
  • Hyperlipidemia due to hepatic lipoprotein synthesis stimulated by decreased plasma oncotic pressure
  • Cumulative thromboembolism risk increased if:
    • Hypovolemia
    • Low serum albumin
    • High protein excretion
    • High fibrinogen levels
    • Low antithrombin III levels
ETIOLOGY
  • Due to primary renal or systemic diseases
  • Membranous nephropathy:
    • Primary cause of nephrotic syndrome in adults
    • Other causes include chronic infection (hepatitis B virus, hepatitis C virus, autoimmune disorders).
    • Renal biopsy shows involvement of all glomeruli.
    • Women have better prognosis.
    • 30% may slowly progress to renal failure.
    • Renal vein thrombosis causes sudden loss of renal function.
    • Treat with steroids and cytotoxic agents in severe cases.
  • Minimal change disease:
    • Most common cause (90%) of nephrotic syndrome in children
    • Other causes: Idiopathic, NSAIDs, paraneoplastic syndrome associated with malignancy (often Hodgkin lymphoma)
    • Best prognosis among all nephrotic syndromes
    • Good response to steroids
  • Focal segmental glomerulosclerosis (FSGS):
    • Young patients (15–30 yr) with nephrotic syndrome
    • Presents with high BP, renal insufficiency, proteinuria, microscopic or gross hematuria.
    • Causes include HIV, heroin abuse, obesity, hematologic malignancies.
    • Primary FSGS responds to steroids.
    • Secondary FSGS treated with ACE inhibitors (ACEI)
    • Collapsing FSGS usually seen in HIV patients
  • Membranoproliferative glomerulonephritis:
    • May present with nephrotic, non-nephrotic, or nephritic sediment
    • Complement levels are persistently low
    • Supportive care: Steroids may be helpful in children.
    • Aspirin and dipyridamole may slow progression.
  • Diabetes mellitus/diabetic nephropathy:
    • Most common secondary cause of nephrotic range proteinuria in adults
    • Microalbuminuria (30–300 mg/24hr) is primary indicator of renal disease.
    • Worsening of renal function in 5–7 yr
    • Does not cause rapid decline in renal function
    • Strict control of blood sugar and ACEI therapy slow progression.
  • Monoclonal gammopathies:
    • Include amyloidosis, multiple myeloma, and light-chain nephropathy
    • Renal manifestations include proteinuria, nephrotic syndrome, nephritic syndrome, and acute renal failure.
    • Lab findings include pseudohyponatremia, low anion gap, hypercalcemia, and Bence Jones proteinuria.
    • Congo red stain of amyloid shows apple green birefringence in polarized light.
    • Supportive care: Steroids and melphalan have some benefit.
  • Systemic lupus erythematosus (SLE):
    • Can present initially as a nephritic process, with progression to nephrotic syndrome
  • HIV-associated nephropathy:
    • FSGS is most common nephropathy.
    • Collapsing glomerulopathy in seropositive HIV carriers with supernephrotic syndrome results in end-stage renal failure that is rapidly progressive (months).
  • Other causes include pre-eclampsia, hepatitis, and drug reactions (culprits include NSAIDs, gold, penicillamine).
DIAGNOSIS
SIGNS AND SYMPTOMS
  • Many patients are asymptomatic.
  • Proteinuria
  • Peripheral edema:
    • Mild pitting edema to generalized anasarca with ascites
  • Hyperlipidemia
  • Lipiduria (urine fatty casts and oval fat bodies)
  • Postural hypotension, syncope, shock
  • Hypertension
  • Hematuria:
    • Microscopic or gross hematuria (secondary to renal vein thrombosis)
  • Renal insufficiency to acute renal failure in some cases
  • Tachypnea, tachycardia, with or without hypotension:
    • Acute onset: Suggests pulmonary embolus (PE), secondary to renal or deep venous thrombosis and hypercoagulable state
    • Up to 30% occurrence of PE in membranous glomerulonephritis
    • Chronic or exertional tachypnea due to:
      • Pulmonary edema
      • Pleural effusions
      • Infection risk due to immunosuppressive treatment and frequent exposure to infections such as Pneumococcus
      • Ascites
  • Protein malnutrition
History
  • Systemic disease such as diabetes, SLE, HIV
  • Use of NSAIDS, gold, or penicillamine
  • History of unintentional weight gain (due to fluid retention)
  • History of “foamy” appearance of urine
Physical-Exam

Varies depending on degree of hypoalbuminemia, hemodynamic status, and etiology of nephrotic syndrome:

  • Edema
  • Hypotension/hypertension
  • Shock
ESSENTIAL WORKUP

Urinalysis:

  • Dipstick protein largely positive:
    • Urine specific gravity >1.025 lowers the diagnostic significance of proteinuria.
  • Microscopic analysis for urinary casts and the presence of cellular elements:
    • Oval fat bodies
    • Free lipid droplets
DIAGNOSIS TESTS & NTERPRETATION
Lab
  • CBC + differential:
    • Anemia common
    • Leukocytosis: Infection
    • Leukopenia: Neoplastic disease or sepsis
    • Thrombocytopenia: Liver disease
  • PT/PTT, international normalized ratio:
    • Coagulation profiles abnormal with concurrent liver disease
  • D
    -dimer, fibrinogen, antithrombin III
    • Suspected thromboembolic event:
      • Often patients are asymptomatic with PE or renal vein thrombosis; therefore need high clinical suspicion.
  • 24-hr urine protein, total protein to creatinine ratio
  • Serum albumin: <3 g/dL
  • Serum total protein
  • Basic metabolic panel with Ca, Mg, P
  • Lipid profile: Elevated total cholesterol, LDL, and VLDL
  • Additional lab tests may be necessary for systemic diseases:
    • Examples include antinuclear antibody, serum and urine protein electrophoresis, hepatitis profile, syphilis, cryoglobulins, complement levels

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