eMedicine Specialties > Nephrology > Glomerular Diseases

Nephrotic Syndrome: Follow-up

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

Follow-up

Further Outpatient Care

  • Long-term management
    • Immunization - Routine immunizations should be delayed until the patient is free of relapses and is off immunosuppression for 3 months. Pneumococcal and influenza vaccines are recommended but are not routinely used, because their efficacy is not established. Children who have received immunosuppressive therapy in the preceding 3 months and are not immune to varicella should receive zoster immunoglobulin if they are exposed to chickenpox or shingles. These patients should also receive acyclovir if they develop chickenpox.
    • Treatment of relapses of steroid-responsive nephrotic syndromes - Most patients experience relapses; data suggest relapse rates of 76-97%, with frequently relapsing rates of up to 50%. The first 2 relapses are treated in the same manner as the initial presentation; frequent relapses are treated with a maintenance dose of prednisone at 0.1-0.5 mg/kg on alternate days for 3-6 months, with the drug then tapered.
    • Monitoring steroid toxicity - Monitoring every 3 months in the outpatient clinic is necessary to help detect adverse effects and to record growth. Supplemental calcium and vitamin D may attenuate bone loss. A yearly checkup is necessary to help detect cataracts.
  • Ongoing use and adjustment of diuretics and angiotensin antagonists are necessary according to the amount of edema and proteinuria that a patient has. This requires periodic monitoring.

Inpatient & Outpatient Medications

  • Other immunosuppressive medications - These medications are usually reserved for steroid-resistant cases in patients who are persistently edematous or for steroid-dependent patients with significant steroid-related adverse effects.
    • Cyclophosphamide may benefit patients who have frequently relapsing steroid-sensitive nephrotic syndrome. Associated complications include bone marrow suppression, hair loss, azoospermia, hemorrhagic cystitis, malignancy, mutations, and infertility.
    • Cyclosporine is indicated when relapses occur after cyclophosphamide treatment. Cyclosporine may be preferable in a pubertal male who is at risk of developing cyclophosphamide-induced azoospermia. Cyclosporine is a highly effective maintenance therapy for patients with steroid-sensitive nephrotic syndrome who are able to stop steroids or take lower doses; however, some evidence suggests that although remission is maintained as long as cyclosporine is administered, relapses are frequent when treatment is discontinued. Cyclosporine can be nephrotoxic and can cause hirsutism, hypertension, and gingival hypertrophy.

Deterrence/Prevention

Amniocentesis may show high levels of alpha-fetoprotein when the fetus has congenital nephrotic syndrome of the Finnish type.31 This may assist in management and counseling.

Complications

  • Infection is a major concern in nephrotic syndrome; patients have an increased susceptibility to infection with Streptococcus pneumoniae, Haemophilus influenzae, Escherichia coli, and other gram-negative organisms. Varicella infection is also common. The most common infectious complications are bacterial sepsis, cellulitis, pneumonia, and peritonitis. Proposed explanations for these complications include decreased immunoglobulin levels, edema fluid acting as a culture medium, protein deficiency, decreased bactericidal activity of the leukocytes, immunosuppressive therapy, decreased perfusion of the spleen caused by hypovolemia, and urinary loss of a complement factor (properdin factor B) that opsonizes certain bacteria.
  • The occurrence of hyperlipidemia may be considered a typical feature of the nephrotic syndrome, rather than a mere complication. It is related to the hypoproteinemia and low serum oncotic pressure of nephrotic syndrome, which then leads to reactive hepatic protein synthesis, including of lipoproteins.32 Some of the elevated serum lipoproteins are filtered at the glomerulus, leading to lipiduria and the classical findings of oval fat bodies and fatty casts in the urine sediment.
  • Atherosclerotic vascular disease appears to occur in greater frequency in subjects with nephrotic syndrome than in healthy subjects of the same age. Curry and Roberts showed that the frequency and extent of coronary artery disease stenoses were greater in patients with nephrotic syndrome than in nonnephrotic control subjects.33 When their study was published (1977), lipid-lowering treatments were less widely used than they are today. Accordingly, the average highest serum total cholesterol in this series was over 400 mg/dL. That is in the range of serum cholesterol seen in familial hypercholesterolemia, a disease that predisposes individuals to myocardial infarction.
  • Hypocalcemia is common in the nephrotic syndrome, but rather than being a true hypocalcemia, it is usually caused by a low serum albumin level. Nonetheless, low bone density and abnormal bone histology are reported in association with nephrotic syndrome. This could be caused by urinary losses of vitamin D – binding proteins, with consequent hypovitaminosis D and, as a result, reduced intestinal calcium absorption. Tessitore et al reported that when the GFR was normal, subjects with the nephrotic syndrome had no consistent calcium or bony abnormalities.34 Yet in that same study, when the GFR was reduced, there were bone mineralization defects found by biopsy.

    A later study found osteomalacia on bone biopsy in over half of adults who had longstanding nephrotic syndrome but whose GFR was preserved.12 A further complication derives from therapies, especially prednisone use. Low bone mass may be found, in relation to cumulative steroid dose.35 This subject remains controversial; as reported by Leonard et al, in 2004, intermittent corticosteroid treatment of childhood steroid-sensitive nephrotic syndrome does not appear to be associated with bone mineral deficits.36 It is possible that long duration of either the nephrotic syndrome or treatments for it are the important risk factors for bone disease in these subjects.
  • Venous thrombosis and pulmonary embolism are well-known complications of the nephrotic syndrome. Hypercoagulability in these subjects appears to derive from urinary loss of anticoagulant proteins, such as anti-thrombin III, compounded by elevations in procoagulant proteins, such as fibrinogen.

    A study by Mahmoodi et al of almost 300 patients with nephrotic syndrome confirmed that venous thromboembolism (VTE) was almost 10 times higher in these persons than in the normal population.11 In the normal population, the average per year incidence of VTE is 0.1-0.2%, whereas among the patients in Mahmoodi's study, the incidence rate reached 1%. Moreover, that risk appeared especially elevated during the first 6 months of nephrotic syndrome, being at almost 10%. This high incidence may justify the routine use of preventive anticoagulation treatment during the first 6 months of a persistent nephrotic syndrome.

    Mahmoodi's study also showed an increased risk of arterial thrombotic events, including coronary and cerebrovascular ones, in nephrotic syndrome. Unlike the risk of VTE, which was related to proteinuria, this arterial risk was related to usual risk factors for arterial disease, such as hypertension, diabetes, smoking, and reduced GFR.
  • Hypovolemia occurs when hypoalbuminemia decreases the plasma oncotic pressure, resulting in a loss of plasma water into the interstitium and causing a decrease in circulating blood volume. Hypovolemia is generally observed only when the patient's serum albumin level is less than 1.5 g/dL. Symptoms include vomiting, abdominal pain, and diarrhea. The signs include cold hands and feet, delayed capillary filling, oliguria, and tachycardia. Hypotension is a late feature.
  • Acute renal failure may indicate an underlying glomerulonephritis but is more often precipitated by hypovolemia or sepsis. Edema of the kidneys that causes a pressure-mediated reduction in the GFR has also been hypothesized.
  • Hypertension related to fluid retention and reduced kidney function may occur.
  • Failure to thrive may develop in patients with chronic edema, including ascites and pleural effusion. Failure to thrive may be caused by anorexia, hypoproteinemia, increased protein catabolism, or frequent infectious complications. Edema of the gut may cause defective absorption, leading to chronic malnutrition.
  • Adverse treatment effects may occur. Corticosteroids and other immunosuppressive drugs have significant adverse effects.

Prognosis

  • The prognosis for patients with primary nephrotic syndrome depends on its cause.
  • The prognosis with congenital nephrotic syndrome is bad. Survival beyond several months is possible only with dialysis and kidney transplantation.
  • Only approximately 20% of patients with focal glomerulosclerosis undergo remission of proteinuria; an additional 10% improve but remain proteinuric. Many patients experience frequent relapses, become steroid-dependent, or become steroid-resistant. End-stage renal disease develops in 25-30% of patients with FSGS by 5 years and in 30-40% of these patients by 10 years.
  • The prognosis for children with minimal-change nephropathy is very good.
    • Most children respond to steroid therapy; still, about 50% of children have 1 or 2 relapses within 5 years and approximately 20% of them continue to relapse 10 years after diagnosis. Only 30% of children never have a relapse after the initial episode. Approximately 3% of patients who initially respond to steroids become steroid-resistant.
    • Poor patient response to steroid therapy may predict a poor outcome, and children who present with hematuria and hypertension are more likely to be steroid-resistant and have a poorer prognosis than are those who do not present with these conditions.
    • In adult nephrotic syndrome, there is a similar variability according to the underlying cause.
    • In adult minimal-change nephropathy, there is a burden of relapse similar to that of children. However, the long-term prognosis for kidney function in patients with this disease is excellent, with little risk of renal failure.
    • As noted, the prognosis of membranous nephropathy is good in terms of patient survival, being the same as that of the unaffected population.
    • In diabetic nephropathy with nephrotic syndrome, there is usually a good response to angiotensin blockade, with reduction of proteinuria to low, sub-nephrotic levels. However, true remission is uncommon. Cardiovascular morbidity and mortality increase as kidney function declines, and some subjects will eventually need dialysis or a kidney transplant.
    • In primary amyloidosis, prognosis is not good, even with intensive chemotherapy. In secondary amyloidosis, remission of the underlying cause, such as rheumatoid arthritis, is followed by remission of the amyloidosis and its associated nephrotic syndrome.

Patient Education

  • Childhood nephrotic syndrome
    • Nephrotic syndrome is a chronic illness characterized by relapses and remissions, which can extend throughout childhood. There will be illness from the disease and from its treatment. Parents may monitor their child's urine and record the results in a diary. The diary can also be used to write down an agreed-upon plan for the management of relapses. Information booklets should be given to the family. Peer support and psychological counseling may be helpful for some families.
    • Progression to renal failure will require preparation for dialysis and/or kidney transplantation.
  • Adult nephrotic syndrome
    • Forms of nephrotic syndrome that cannot be cured may evolve into renal failure and the need for dialysis or kidney transplantation.

Miscellaneous

Medicolegal Pitfalls

  • A study using the Cochrane database has put into question whether prednisone treatment is beneficial in adult minimal-change nephropathy.37 Nonetheless, when the nephrotic syndrome causes illness, by uncomfortable edema or associated coagulopathy, treatment would appear needed.
  • The role of preventive anticoagulation in nephrotic syndrome has been reported, but there is no proof that it is beneficial.
  • Hyperlipidemia occurs in nephrotic syndrome, and it can be controlled with lipid-lowering agents. Older studies have reported a predisposition to atherosclerosis in patients with nephrotic syndrome, but there is no evidence-based proof that lipid-lowering drugs improve renal or patient outcomes.

Special Concerns

  • A better understanding of the mechanisms of nephrotic syndrome may greatly change the management of the disease. For example, confirmation of the role of galactose in some forms of focal glomerulosclerosis may lead to novel and better treatments.38
 


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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