Warung Bebas

Thursday, 9 September 2010

Nephrotic syndrome Part 1


Patient asks to Mbah Dukun: "Mbah, would you explain about Nephrotic Syndrome?"
Mbah Dukun Bagong answers: " Sure, ok read the text below"

Nephrotic syndrome (NS) is one of the clinical manifestations of glomerulonephritis (GN) are marked with anasarka edema, massive proteinuria ≥ 3.5 g / dl, hypercholesterolemia and lipiduria. At the beginning of the process or the mild NS stage, to make the diagnosis, not all symptoms must be found. Massive proteinuria is a typical sign of NS, but in severe NS accompanied low serum albumin concentration, excretion of protein in urine was also reduced. Proteinuria also contributes to various complications that occur in the NS. Not only Proteinuria,hypoalbuminemia, hiperlipidemia and lipiduria also found in NS. Nitrogen balance diorders, hypercoaguloability, disturbances of calcium and bone metabolism, and thyroid hormones are often found in NS. Generally, NS with normal renal function can heal itself and showed a good response to steroid therapy. However, for some cases develop into end stage renal disease or develop inti chronic.


Patient asks to Mbah Dukun: "Mbah, what are cause of NS?"
Mbah Dukun Bagong answers:
Nephrotic syndrome can be caused by primary and secondary Glomerulonephritis.
A. Primary Glomerulonephritis
  • GN with minimal lessions
  • Glomerulosclerotic focal
  • Membranous Glomerulonephritis
  • GN membranoproliferatif
  • Other proliferative
B. Secondary Glomerulonephritis

1. Infections:
  • HIV, Hepatitis B and C virus
  • Syphilis, Malaria
  • TBC, Leprosy
2. Malignancy:
  • Adenosarcoma
  • Lymphoma
  • Multiple Myeloma
  • Renal Carcinoma
3. Connective Tissue Disease:
  • SLE
  • Rhematoid Arthritis
  • Mixed Cinnective Tissue Disease
4. Drugs and Toxins:
  • NSIDs
  • Gold Preparations
  • Penicillamine
  • Probenecid
  • Mercury
  • Captopril
  • Heroin
5. Other:
  • Diabetes Mellitus
  • Amyloidosis
  • Pre-Eclampsia
  • Vesikoureter reflux
  • Primary or idiopathic Glomerulonephritis is the most frequent cause of NS. in Primary GN, histopathological abnormality was found. Due to secondary causes such as infections that are often encountered in post infectious GN Stretococcus or Hepatitis B virus infection, caused by medications such as non steroidal anti-inflammatory drugs or preparations of organic gold, and caused by systemic disease.

Patient asks to Mbah Dukun: "Mbah, tell me about patophysiology of NS?"
Mbah Dukun Bagong answers:

1. Proteinuria
Proteinuria caused by increased capillary permeability to proteins due to glomerulus damage. Normally, Glomerular basement membrane (GBM) has a barrier mechanism to prevent leakage of protein. The first barrier mechanism based on moleculear size (size barrier) and the second based on electrical charge. In the NS, two mechanism are invloved disrupted. Besides the configuration of protein molecules also determine wether the protein passes through the GBM. Proteinuria is divided into selective and non-selective based on size of protein molecules that come out through urine. Selective proteinuria outif a protein consisits of small molecules such as albumin, while non-selective when the protein comes out such a large molecule composed of immunoglobulin. selectivity of proteinuria determined by GBM structural integrity. In the NS which caused by GN Minimal Lessions, found selective proteinuria. Electron microscope examination showed fusion of foot processor glomerular visceral epithelial cells and the released of cells from GBM structure. In Glomerulosclerotic Focal, GBM increased permeability caused by a factor involved in the circulation. These factors lead to glomerular visceral epithelial cells regardless of GBM that permeability increases. In Glomerulonephritis Membranous, GBM structural are damage caused by immune complex deposition in the sub-epithelium.
2. Hypoalbuminemia
Plasma Albumin concetration determined by protein intake, Liver albumin synthesis, and loss of protein through urine. Hypoalbuminemia is caused by masive proteinuria due to reduced plasma oncotic presure. To maintain plasma oncotic pressure, the liver increases production of albumin. Improvement of liver albumin synthesis was not succesfully to block the emergence hypoalbuminemia. High protein diet can improve liver albumin synthesis, but it may encourage increased excretion of albumin in the urine. Hypoalbuminemia may also occur due to increased reabsorption and catabolism of albumin by the proximal tubule.
3. Edema
Edema can be explained by theory of UNDERFILL and OVERFILL.
  • Underfill theory explains that hypoalbuminemia is a factor of edema of NS. Hypoalbuminemia caused a decrease in plasma oncotic pressure so that fluid shifts from intravascular to the network interstitium and edema. Consequent of Oncotic pressure drop due to plasma and plasma fluid shift occurs hypovolemia and to compnsate by increasing renal sodium and water retention. These compensatory mechanisms will improve intravascularvolume but will also excerbates occurence of edema increasingly hypoalbuminemia so continues. 
  • Overfill theory explains that the retention of sodium as a primary renal defect. retention of Sodium by the kidneys causes increased extracelluler fluid causing edema. Decrease of GFR (glomerulus filtrate rate) due to kidney damage would increase the occurence of sodium retention and edema. Both mechanism found together in patients with NS. 

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