Minimal-change disease (MCD) causes intense proteinuria, edema, and intravascular volume depletion due to glomerular lesions.
It is the most common nephrotic syndrome in children and occurs in adults too. “Minimal change” disease shows no significant abnormalities in kidney biopsies.
Laboratory tests may show profound proteinuria and oval fat bodies, with diagnostic thresholds at over 40 mg/h/m2 in children and 3.5 g/d/1.73 m2 in adults.
MCD is hypothesized as a T cell disorder causing cytokine to release those damages glomerular epithelial foot processes and reduces polyanion synthesis.
Polyanions create charge barrier against macromolecule filtration, e.g., albumin.
Damaged polyanions lead to albumin leakage with hemopexin suggested as the potential permeability factor.
Epidemiology
Minimal-change nephrotic syndrome accounts for 85-95% of pediatric cases, 50% in adolescents, and 10-15% in adults with nephrotic syndrome.
Nephrotic syndrome occurs in 2-7 new cases and has 15 cases per 100,000 children. MCD occurs more in boys than girls in children, but equally in adults.
MCD incidences peak in children at age 2, with 80% diagnosed before age 6. Hypertension affects about 30% of adults more than 60 years old.
Anatomy
Pathophysiology
Interleukin-4 levels rise in active phase blood monocytes and normalize in remission. Higher synaptopodin in podocytes improves steroid therapy response.
Cytokine overproduction causes altered glomerular permeability and selective proteinuria without significant inflammation.
Patients with acute kidney injury show elevated endothelin 1 expression in glomeruli, vessels, and tubules with podocytes and slit diaphragms for proteinuria development.
B-cell–depleting agents indicate B-cells’ involvement in MCD pathogenesis and treatment efficacy.
Etiology
The causes of MCD are:
Primary (Idiopathic)
Immune or Allergic Causes
Hypersensitivity reactions
Medications
Genetics
Prognostic Factors
Antibiotics, glucocorticoids, and organized management schedules lowered MCD mortality rates.
A review of 95 adults with AKI showed older, hypertensive patients had lower serum albumin and more proteinuria than non-AKI patients.
Patients with nephrotic syndrome show higher rates of thromboemboli, deep vein and renal vein thrombosis are more common in membranous nephropathy than MCD.
Higher glomerular filtration rate increased relapse risk, with early relapse more common in women.
Clinical History
Collect details including presenting symptoms, family and medical history to understand clinical history of patient.
Physical Examination
Cardiovascular Examination
Respiratory Examination
Abdominal Examination
Genitourinary Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Symptoms in children:
Periorbital and generalized edema, fatigue, frothy urine
Symptoms in adults:
weight gain, thromboembolic events, cellulitis, pneumonia, acute kidney injury
Differential Diagnoses
Focal Segmental Glomerulosclerosis
Membranous Nephropathy
Diabetic Nephropathy
Lupus Nephritis
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
High prevalence of minimal-change disease in pediatric nephrotic syndrome prompts an initial corticosteroid trial, which causes complete remission of proteinuria.
MCD from Hodgkin lymphoma often resists steroids but improves with primary disease treatment. Persistent proteinuria after relapses necessitates tissue diagnosis before cytotoxic or immunosuppressive therapy.
In adolescents and adults, response occurs in 80%-90% of cases with remission required 16 weeks.
Hypovolemia requires immediate volume expansion with purified plasma protein and isotonic saline while parenteral albumin is not suitable long-term.
Diuretics are recommended for severe edema cases with respiratory or gastrointestinal symptoms and activity restrictions.
Prevent thrombotic episodes with mobilization and careful venipuncture techniques.
Procedures such as kidney biopsy is primary diagnostic option, while interventions options including paracentesis, thoracentesis, and dialysis to manage complications of MCD.
use-of-phases-in-managing-minimal-change-disease
In the acute diagnosis phase, the focus is to achieve remission of nephrotic syndrome, prevent and manage complication.
Pharmacologic therapy is effective in the treatment phase as it includes the use of diuretics, corticosteroids, antineoplastic agents, and immunosuppressant agents.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the nephrologist are scheduled to check the improvement of patients along with treatment response.
Minimal-change disease (MCD) causes intense proteinuria, edema, and intravascular volume depletion due to glomerular lesions.
It is the most common nephrotic syndrome in children and occurs in adults too. “Minimal change” disease shows no significant abnormalities in kidney biopsies.
Laboratory tests may show profound proteinuria and oval fat bodies, with diagnostic thresholds at over 40 mg/h/m2 in children and 3.5 g/d/1.73 m2 in adults.
MCD is hypothesized as a T cell disorder causing cytokine to release those damages glomerular epithelial foot processes and reduces polyanion synthesis.
Polyanions create charge barrier against macromolecule filtration, e.g., albumin.
Damaged polyanions lead to albumin leakage with hemopexin suggested as the potential permeability factor.
Minimal-change nephrotic syndrome accounts for 85-95% of pediatric cases, 50% in adolescents, and 10-15% in adults with nephrotic syndrome.
Nephrotic syndrome occurs in 2-7 new cases and has 15 cases per 100,000 children. MCD occurs more in boys than girls in children, but equally in adults.
MCD incidences peak in children at age 2, with 80% diagnosed before age 6. Hypertension affects about 30% of adults more than 60 years old.
Interleukin-4 levels rise in active phase blood monocytes and normalize in remission. Higher synaptopodin in podocytes improves steroid therapy response.
Cytokine overproduction causes altered glomerular permeability and selective proteinuria without significant inflammation.
Patients with acute kidney injury show elevated endothelin 1 expression in glomeruli, vessels, and tubules with podocytes and slit diaphragms for proteinuria development.
B-cell–depleting agents indicate B-cells’ involvement in MCD pathogenesis and treatment efficacy.
The causes of MCD are:
Primary (Idiopathic)
Immune or Allergic Causes
Hypersensitivity reactions
Medications
Antibiotics, glucocorticoids, and organized management schedules lowered MCD mortality rates.
A review of 95 adults with AKI showed older, hypertensive patients had lower serum albumin and more proteinuria than non-AKI patients.
Patients with nephrotic syndrome show higher rates of thromboemboli, deep vein and renal vein thrombosis are more common in membranous nephropathy than MCD.
Higher glomerular filtration rate increased relapse risk, with early relapse more common in women.
Collect details including presenting symptoms, family and medical history to understand clinical history of patient.
Cardiovascular Examination
Respiratory Examination
Abdominal Examination
Genitourinary Examination
Symptoms in children:
Periorbital and generalized edema, fatigue, frothy urine
Symptoms in adults:
weight gain, thromboembolic events, cellulitis, pneumonia, acute kidney injury
Focal Segmental Glomerulosclerosis
Membranous Nephropathy
Diabetic Nephropathy
Lupus Nephritis
High prevalence of minimal-change disease in pediatric nephrotic syndrome prompts an initial corticosteroid trial, which causes complete remission of proteinuria.
MCD from Hodgkin lymphoma often resists steroids but improves with primary disease treatment. Persistent proteinuria after relapses necessitates tissue diagnosis before cytotoxic or immunosuppressive therapy.
In adolescents and adults, response occurs in 80%-90% of cases with remission required 16 weeks.
Hypovolemia requires immediate volume expansion with purified plasma protein and isotonic saline while parenteral albumin is not suitable long-term.
Diuretics are recommended for severe edema cases with respiratory or gastrointestinal symptoms and activity restrictions.
Prevent thrombotic episodes with mobilization and careful venipuncture techniques.
Nephrology
Patient should include low-sodium diet to reduce edema by minimizing fluid retention.
Ensure vaccinations are up to date to reduce infection risk. Patient should follow proper handwashing and general hygiene practices.
Avoid exposure to crowded areas during active disease or immunosuppressive therapy.
Proper awareness about MCD should be provided and its related causes with management strategies.
Appointments with a nephrologist and preventing recurrence of disorder is an ongoing life-long effort.
Nephrology
Furosemide:
It blocks the sodium reabsorption in the thick ascending limb of the loop of Henle.
Nephrology
Prednisone:
It has an anti-inflammatory effect that inhibits inflammatory mediator gene transcription.
Nephrology
Cyclophosphamide:
It interferes with DNA due to alkylation and cross-linking strands of DNA.
Nephrology
Cyclosporine A:
It inhibits production and release of IL-2–mediated activation of T lymphocytes.
Chlorambucil:
It interferes with DNA replication and RNA transcription.
Tacrolimus:
It inhibits T-cell activation and proliferation due to humoral immunity.
Nephrology
Levamisole:
It stimulates formation of antibodies to increase the response of T-cell.
Nephrology
Procedures such as kidney biopsy is primary diagnostic option, while interventions options including paracentesis, thoracentesis, and dialysis to manage complications of MCD.
Nephrology
In the acute diagnosis phase, the focus is to achieve remission of nephrotic syndrome, prevent and manage complication.
Pharmacologic therapy is effective in the treatment phase as it includes the use of diuretics, corticosteroids, antineoplastic agents, and immunosuppressant agents.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the nephrologist are scheduled to check the improvement of patients along with treatment response.
Minimal-change disease (MCD) causes intense proteinuria, edema, and intravascular volume depletion due to glomerular lesions.
It is the most common nephrotic syndrome in children and occurs in adults too. “Minimal change” disease shows no significant abnormalities in kidney biopsies.
Laboratory tests may show profound proteinuria and oval fat bodies, with diagnostic thresholds at over 40 mg/h/m2 in children and 3.5 g/d/1.73 m2 in adults.
MCD is hypothesized as a T cell disorder causing cytokine to release those damages glomerular epithelial foot processes and reduces polyanion synthesis.
Polyanions create charge barrier against macromolecule filtration, e.g., albumin.
Damaged polyanions lead to albumin leakage with hemopexin suggested as the potential permeability factor.
Minimal-change nephrotic syndrome accounts for 85-95% of pediatric cases, 50% in adolescents, and 10-15% in adults with nephrotic syndrome.
Nephrotic syndrome occurs in 2-7 new cases and has 15 cases per 100,000 children. MCD occurs more in boys than girls in children, but equally in adults.
MCD incidences peak in children at age 2, with 80% diagnosed before age 6. Hypertension affects about 30% of adults more than 60 years old.
Interleukin-4 levels rise in active phase blood monocytes and normalize in remission. Higher synaptopodin in podocytes improves steroid therapy response.
Cytokine overproduction causes altered glomerular permeability and selective proteinuria without significant inflammation.
Patients with acute kidney injury show elevated endothelin 1 expression in glomeruli, vessels, and tubules with podocytes and slit diaphragms for proteinuria development.
B-cell–depleting agents indicate B-cells’ involvement in MCD pathogenesis and treatment efficacy.
The causes of MCD are:
Primary (Idiopathic)
Immune or Allergic Causes
Hypersensitivity reactions
Medications
Antibiotics, glucocorticoids, and organized management schedules lowered MCD mortality rates.
A review of 95 adults with AKI showed older, hypertensive patients had lower serum albumin and more proteinuria than non-AKI patients.
Patients with nephrotic syndrome show higher rates of thromboemboli, deep vein and renal vein thrombosis are more common in membranous nephropathy than MCD.
Higher glomerular filtration rate increased relapse risk, with early relapse more common in women.
Collect details including presenting symptoms, family and medical history to understand clinical history of patient.
Cardiovascular Examination
Respiratory Examination
Abdominal Examination
Genitourinary Examination
Symptoms in children:
Periorbital and generalized edema, fatigue, frothy urine
Symptoms in adults:
weight gain, thromboembolic events, cellulitis, pneumonia, acute kidney injury
Focal Segmental Glomerulosclerosis
Membranous Nephropathy
Diabetic Nephropathy
Lupus Nephritis
High prevalence of minimal-change disease in pediatric nephrotic syndrome prompts an initial corticosteroid trial, which causes complete remission of proteinuria.
MCD from Hodgkin lymphoma often resists steroids but improves with primary disease treatment. Persistent proteinuria after relapses necessitates tissue diagnosis before cytotoxic or immunosuppressive therapy.
In adolescents and adults, response occurs in 80%-90% of cases with remission required 16 weeks.
Hypovolemia requires immediate volume expansion with purified plasma protein and isotonic saline while parenteral albumin is not suitable long-term.
Diuretics are recommended for severe edema cases with respiratory or gastrointestinal symptoms and activity restrictions.
Prevent thrombotic episodes with mobilization and careful venipuncture techniques.
Nephrology
Patient should include low-sodium diet to reduce edema by minimizing fluid retention.
Ensure vaccinations are up to date to reduce infection risk. Patient should follow proper handwashing and general hygiene practices.
Avoid exposure to crowded areas during active disease or immunosuppressive therapy.
Proper awareness about MCD should be provided and its related causes with management strategies.
Appointments with a nephrologist and preventing recurrence of disorder is an ongoing life-long effort.
Nephrology
Furosemide:
It blocks the sodium reabsorption in the thick ascending limb of the loop of Henle.
Nephrology
Prednisone:
It has an anti-inflammatory effect that inhibits inflammatory mediator gene transcription.
Nephrology
Cyclophosphamide:
It interferes with DNA due to alkylation and cross-linking strands of DNA.
Nephrology
Cyclosporine A:
It inhibits production and release of IL-2–mediated activation of T lymphocytes.
Chlorambucil:
It interferes with DNA replication and RNA transcription.
Tacrolimus:
It inhibits T-cell activation and proliferation due to humoral immunity.
Nephrology
Levamisole:
It stimulates formation of antibodies to increase the response of T-cell.
Nephrology
Procedures such as kidney biopsy is primary diagnostic option, while interventions options including paracentesis, thoracentesis, and dialysis to manage complications of MCD.
Nephrology
In the acute diagnosis phase, the focus is to achieve remission of nephrotic syndrome, prevent and manage complication.
Pharmacologic therapy is effective in the treatment phase as it includes the use of diuretics, corticosteroids, antineoplastic agents, and immunosuppressant agents.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the nephrologist are scheduled to check the improvement of patients along with treatment response.
Both our subscription plans include Free CME/CPD AMA PRA Category 1 credits.
Digital Certificate PDF
On course completion, you will receive a full-sized presentation quality digital certificate.
medtigo Simulation
A dynamic medical simulation platform designed to train healthcare professionals and students to effectively run code situations through an immersive hands-on experience in a live, interactive 3D environment.
medtigo Points
medtigo points is our unique point redemption system created to award users for interacting on our site. These points can be redeemed for special discounts on the medtigo marketplace as well as towards the membership cost itself.
Community Forum post/reply = 5 points
*Redemption of points can occur only through the medtigo marketplace, courses, or simulation system. Money will not be credited to your bank account. 10 points = $1.
All Your Certificates in One Place
When you have your licenses, certificates and CMEs in one place, it's easier to track your career growth. You can easily share these with hospitals as well, using your medtigo app.
