Read Rosen & Barkin's 5-Minute Emergency Medicine Consult Online

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

Tags: #Medical, #Emergency Medicine

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

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
12.34Mb size Format: txt, pdf, ePub
ads
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
BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
12.34Mb size Format: txt, pdf, ePub
ads

Other books

Ranchero by Gavin, Rick
The Ghost Hunters by Neil Spring
The Undertow by Jo Baker
Firebrand by Antony John
Pagan Lover by Anne Hampson
Stonewall by Martin Duberman