eMedicine Specialties > Nephrology > Glomerular Diseases

Nephrotic Syndrome: Differential Diagnoses & Workup

Author: Eric P Cohen, MD, Professor of Medicine, Nephrology Fellowship Program Director, Department of Medicine, Division of Nephrology, Medical College of Wisconsin; Nephrology Section Chief, Zablocki Veterans Affairs Hospital
Contributor Information and Disclosures

Updated: Aug 25, 2009

Differential Diagnoses

Diabetic Nephropathy
Light Chain-Associated Renal Disorders
Focal Segmental Glomerulosclerosis
Minimal-Change Disease
Glomerulonephritis, Acute
Nephritis, Radiation
Glomerulonephritis, Chronic
Sickle Cell Nephropathy
Glomerulonephritis, Membranous
HIV Nephropathy
IgA Nephropathy

Other Problems to Be Considered

Heart failure may cause a similar presentation to that of nephrotic syndrome. In typical cases of heart failure, however, there will be a history of heart disease and/or features of poor heart function on exam, such as a third heart sound and even low blood pressure. In heart failure without kidney disease, there will be little or no proteinuria. Nephrotic syndrome with renal impairment, such as may occur in IgA nephropathy, may cause secondary reduction in heart function, with cardiomegaly on exam. Such cases would typically be hypertensive and there will be substantial proteinuria on urinalysis. 

Subjects with cirrhosis may have substantial fluid retention, both as ascites and as peripheral edema. Unless there is associated kidney disease, however, there will be little or no proteinuria in cirrhosis.

Workup

Laboratory Studies

  • Urinalysis is the first test used in the diagnosis of nephrotic syndrome.
    • Nephrotic range proteinuria will be apparent by 3+ or 4+ readings on the dipstick, or by semiquantitative testing by sulfosalicylic acid. A 3+ reading is 300 mg/dL of urinary protein or more, which is 3 g/L or more and thus in the nephrotic range. The chemistry of the dipsticks is such that albumin is the major protein that is tested.
    • Glucosuria points to diabetes.
    • The urine sediment exam may show cells and/or casts.
    • Waxy casts mark proteinuric renal disease. By use of a polarizing microscope, one can see oval fat bodies and also fatty casts. These point to the nephrotic syndrome. They occur because of glomerular filtration of lipoproteins, the uptake of these by the tubular cells that then fall off into the urine. Viewed by polarizer, the oval fat bodies and fatty casts cause a "Maltese cross" appearance.
    • The presence of more than 2 red blood cells (RBCs) per high power field is indicative of microhematuria. Microhematuria may occur in membranous nephropathy but not in minimal-change nephropathy. Glomerular disease may allow RBCs to traverse the damaged glomerular basement membrane, and the RBCs in the sediment may then be deformed, or dysmorphic. This points to glomerular disease with inflammation and destruction of the normal structures, ie, a nephritis (and thus a nephritic picture). This could occur in, for example, nephrotic syndromes associated with IgA nephropathy or proliferative glomerulonephritis.
    • More than 2 granular casts in the entire sediment is a biomarker for renal parenchymal disease. Variable-caliber granular casts point to reduced renal function.
  • Urinary protein is measured by a timed collection or a single, spot collection.28 A timed collection is typically done over a 24-hour period, starting at 7 am and finishing the next day at the same time. In healthy individuals, there are no more than 150 mg of total protein in a 24-hour urine collection. A single, spot urine collection is much easier to obtain. When the ratio of urine protein to urine creatinine is greater than 2 g/g, this corresponds to 3 grams of urine protein per day or more.
  • The exact type of urine protein is of potential interest. This can be tested by urine protein electrophoresis. Proteinuria that does not include albumin may point to overflow proteinuria that occurs in paraproteinemias, such as multiple myeloma. There has been intermittent interest in establishing whether proteinuria is "selective" for albumin, being more than 85% composed of albumin, as opposed to nonselective. In the case of selective proteinuria, there could be a charge-selective leak of albumin across the glomerular barrier, perhaps due to reduced negative charges on that barrier, whereas nonselective proteinurias would point to more substantial glomerular injury and perhaps also to lesser response to prednisone treatment.
  • Serum tests for kidney function are essential. Serum creatinine will be in the normal range in uncomplicated nephrotic syndrome, such as that occurring in minimal-change nephropathy. In children, the serum creatinine level will be lower than it is in adults. The normal adult serum creatinine level is approximately 1 mg/dL, whereas that of a child aged 5 years will be about 0.5 mg/dL. Values higher than this indicate reduced kidney function.  
  • The serum albumin is classically low in nephrotic syndrome, being below its normal range of 3.5-4.5 g/dL. A single-center study showed that when a patient's serum albumin level was normal, rather than low, focal glomerulosclerosis, rather than other conditions, tended to be the cause of nephrotic syndrome.29

Imaging Studies

  • Ultrasonographic scanning can be used to determine whether a patient possesses 2 kidneys and to demonstrate their echogenicity. Individuals with a single kidney may be prone to developing focal glomerulosclerosis. Having only 1 kidney is also a relative contraindication to kidney biopsy. Increased renal echogenicity by ultrasonography is consistent with intrarenal fibrosis, ie, chronic disease with reduced kidney function.

Other Tests

  • In infants with nephrotic syndrome, genetic testing for the NPHS1 and NPHS2 mutations may be useful. These are mutations of nephrin and podocin, respectively. In children with steroid-resistant nephrotic syndrome, testing for the NPHS2 mutation may be indicated.
  • In adults with nephrotic syndrome, tests for hepatitis B and C, HIV, and even syphilis may be useful. Tests for lupus, including ANA, anti-dsDNA, and complement, may be useful. Testing for antineutrophil cytoplasmic antibodies (ANCA) is not indicated in typical nephrotic syndrome, because that test is associated with rapidly progressive glomerulonephritis, which presents with a nephritic picture rather than one that is typically nephrotic. Tests for previous streptococcal infection, such as antistreptolysin O, are not usually indicated for nephrotic syndrome, since postinfectious glomerulonephritis usually causes a nephritic picture, not nephrotic syndrome.
  • Future studies for urinary biomarkers by which the cause and severity of nephrotic syndrome may be identified may become available.30

Procedures

  • For childhood nephrotic syndrome, a renal biopsy is indicated for the following:
    • Congenital nephrotic syndrome
    • Children older than 8 years at onset
    • Steroid resistance
    • Frequent relapses or steroid dependency
    • Significant nephritic manifestations
  • Adult nephrotic syndrome of unknown origin may require a renal biopsy for diagnosis.
  • A renal biopsy is not indicated in adults when nephrotic syndrome is due to an obvious cause, such as diabetes mellitus. Thus, a subject with diabetes, diabetic retinopathy, and the nephrotic syndrome may well have diabetic nephropathy and not need to undergo kidney biopsy.
  • Abdominal fat-pad biopsy or gingival biopsy
    • May be useful in adult patients to help diagnose either primary or secondary amyloidosis

Histologic Findings

Histologic findings in nephrotic syndrome are determined by the disease's cause. It is worth noting that in clinical experience, glomerular disease has been found to cause of nephrotic-range proteinuria, not tubular disease. This appears to contradict the proposal that tubular function determines proteinuria.7

Staging

There are histopathologic stages for membranous nephropathy but not for other causes of nephrotic syndrome.

More on Nephrotic Syndrome

Overview: Nephrotic Syndrome
Differential Diagnoses & Workup: Nephrotic Syndrome
Treatment & Medication: Nephrotic Syndrome
Follow-up: Nephrotic Syndrome
Multimedia: Nephrotic Syndrome
References
Further Reading
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Keywords

nephrotic syndrome, nephrotic, syndrome nephrotic, nephrosis, nephropathy, proteinuria, diabetic nephropathy, glomerulosclerosis, IgA nephropathy, focal segmental glomerulosclerosis, focal glomerulosclerosis, membranous nephropathy, minimal change disease, minimal-change disease, hypoalbuminemia, hypercholesterolemia, minimal change nephropathy, pediatric nephrotic syndrome, collagen vascular disease, IgA nephropathy, amyloidosis, congenital nephrotic syndrome Finnish type, focal segmental glomerulosclerosis

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Contributor Information and Disclosures

Author

Eric P Cohen, MD, Professor of Medicine, Nephrology Fellowship Program Director, Department of Medicine, Division of Nephrology, Medical College of Wisconsin; Nephrology Section Chief, Zablocki Veterans Affairs Hospital
Eric P Cohen, MD is a member of the following medical societies: American Society of Nephrology, Central Society for Clinical Research, International Society of Nephrology, and Radiation Research Society
Disclosure: Nothing to disclose.

Medical Editor

Laura L Mulloy, DO, FACP, Professor of Medicine, Chief, Section of Nephrology, Hypertension and Transplantation Medicine, Glover/Mealing Eminent Scholar Chair in Immunology, Medical College of Georgia
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

 
 
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