Glomerular Diseases Causes Clinical Presentation Symptoms Etiology Treatment

Glomerular Diseases

Some Type of Glomerular Diseases –

  • Focal glomerular disease
    • involves less than 50% of glomeruli.
  • Diffuse glomerular disease
    • involves more than 50% of glomeruli.
  • Glomerular disease may be segmental or global
    •  depending on whether the glomerular tuft is involved partially or wholly.
  • Membranous glomerulonephritis
    • means deposi­tion of immune substances on the glomerular base­ment membrane.
  • Glomerulosclerosis
    • means increase of extracellu­lar material in GBM(glomerular basement memb::ane) and mesangium.
  • Glomerular fibrosis
    • means deposition of collagen due to healing of crescents resulting in tubulo-in­terstitial disease.
  • Proliferative disease
    • may be true proliferation of glom ruli or hypercellularity due to infiltration of leu­kocytes
  • Endocapifiaty or intracapillary disease
    • means mesangial cells”are involved.
  • Crescentric glomerular disease
    • is a half-moon shaped collection of cells in Bowman’s space.
  • It is also called rapidly progressive glomerulo-nephri­tis because of its rapid course.

CLINICAL PRESENTATION OF GLOMERULAR DISEASE —

TYPES OF GLOMERULAR DISEASES Diffuse proliferative glomerulonephritis

  • There is acute nephritic syndrome – red blood cells, RBC casts, leukocytes, subnephrotic proteinuria <3 g in 24 hours.
  • There is acute renal failure over days to weeks with hypertension, edema, oliguria, active urine sediments, subnephrotic proteinuria.

Etiology –

Treatment

  • Antibiotics, Supportive therapy, Diuretics and antihypertensives, Dialysis.
  • Prognosis is good in post-streptococcal GN-resolution occurs in 6-8 weeks.
  • There may be proteinuria for 1 year or more.
  • In SLE – treatment of lupus nephritis after renal bi­opsy.
  • For extrarenal manifestations in SLE- give glucocorti­coids, salicylates, antimalarials, cyclophosphamide.

Crescentric GN (CGN) or Rapidly Progressive GN (RPGN)

  • There is subacute renal failure over weeks to months, active urine sediment, hypertension, edema, oliguria and proteinuria.

Etiology

  • Immune complexes, Wegener’s granulomatosis, pol­yarteritis nodosa.

Treatment

Focal proliferative GN

  • There is mild to moderate glomerular infiltration.
  • There is active urinary sediment and mild decline in GFR.

Etiology

  • All ,the diseases which cause diffuse proliferative or RPGN can cause focal proliferative GN, IgA nephr­opathy.

Treatment

  • Spontaneous remission does not occur.
  • Glucocorti­coids for 8 weeks may cause decrease in proteinuria.
  • Glucocorticoids is given for 24 weeks.
  • Cyclophosphamide and Cyclosporin may be given.
  • Renal transplantation is the ultimate treatment.

Mesangioproliferative GN

Etiology

Treatment

  • Immunosuppressive drugs, dialysis and renal trans­plant.

Membrano proliferative GN

  • There is nephritic- and nephrotic picture, decline in GFR, active urine s’ediment, and proteinuria in neph­rotic range.

Etiology

  • Immune complex, thrombotic microangiopathies, deposition diseases, post renal or marrow transplan­tation.

Minimal change GN

  • It is a common renal disease in children.
  • It is also called nil disease, lipoid nephrosis, foot pro­cess disease. Glomerular size and architecture are normal.
  • Presentation is nephrotic syndrome with proteinuria more than 3.5 gjday, hypoalbuminemia, edema, hy­perlipidemia, thrombotic diathesis and decline in GFR upto 30%.
  • There is benignPheochromocytoma Clinical Features Diagnosis Treatment. Read more ... » urinary sediment.
  • There may be microscopic hematuria. Hypertension is rare.

Etiology

Treatment

  • It is highly steroid-responsive, prognosis is excellent.
  • Steroids are given for 20 – 24 wks, 1-1.5 mgjkg body weight j day for 4 wks, followed by 1 mg jkg j day on alternate days for 4 wks.
  • Treatment may be given up to 6 months. Relapse may occur.
  • Cyclosporin, azathioprine may also be given especially in steroid-resistant cases.

Focal segmental glomerulosclerosis

  • There is nephrotic syndrome

Etiology

  • Idiopathic, secondary response to nephron injury.

Treatment

  • Treat nephrotic syndrome

Nodular or global sclerosis

  • There is proteinuria and chronic renal failure

Etiology

  • Diabetic nephropathy and other glomerulopathies.
  • Nephropathy occurs in 30% of type I DM and 20% of type II DM,
  • Among patients of ESRD, type II DM is a very com­mon cause because of the high incidence of type II DM worldwide.
  • The risk factors for diabetic nephropathy are hyperg­Iycemia, hypertension, proteinuria, cigarette smok­ing, hyperlipidemia.

Treatment

Membranous GN

  • There is nephrotic syndrome,

Etiology “,

  • Idiopathic, infections-hepatitis Band C, Malarra, Lep­rosy, Schistomiasis, drugs (gold, Captopr:il5, autoim­mune diseases-SLE, Rheumatuid arthritis, Paraneoplastic diseases.

Treatment

Deposttlon diseases

  • There”is nephritic and nephrotic presentation with renal failure over the years.

Etiology

  • Amyloid, cryoglobulinemia.

Treatment

  • Colchicine, melphalan, prednisolone, stem cell trans­plantation.

Thrombotic microangiopathy

  • There is renal failure (usually acute), hypertension, proteinuria. Urine contains RBCs.

Etiolgy

Treatment

  • Treat etiology and mange renal failure.

Non-immune basement membrane abnormali­ties

  • There is hematuria and renal failure.

Etiogy

Alports syndrome -

  • Hereditary nephritis, mesangial hypercellularity, focal and segmental glomeruloscle­rosis, damage of GBM (Glomerular Basement Mem­brane), progresses to ESRD.
  • Treatment of Alport’s syndrome is ACE inhibitors, di­alysis, transplantation.
  • Nail-patella\~yndrome - Hereditary autosomal dominant disorder, multiple bony abnormalities of el­bows, knees, nail dysplasia, GBM thickening, inter­stitial fibrosis, glomerular sclerosis.
  • The disease manifests with hematuria, proteinuria. Progression to ESRD in some cases.

Waldenstrom’s Macroglobulinemia

IgA nephropathy (Berger’s disease)

  • It is a very common nephropathy – glomerulopdthy, with idiopathic etiology like Henoch-Schonlein pur­pura.
  • It is found in association with chronic liver disease, idiopathic pneumonia, ankylosing spondylitis, Sjogren’s syndrome.

Sickle cell disease

Drugs which may cause Glomerulopathy Minimal change disease -

Membranous nep.hropathy -

  • Gold, Mercury, Captopril, Penicillamine

Necrotizing glomerulonephritis -

  • Ciprofloxacin Proliferative glomerulonephritis with vasculitis­
  • Sulphonamide, Thiazides, Allopurinol, Penicillin.

RPGN (Rapidly Progressive Glomerulonephri­tis)-

  • Rifampicin, Warfarin, Penicillamine, Amoxycillin, Carbimazole.

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