SINDROM NEFROTIK

ReferatSamuel Marco 0710160

Melisa C

• Nephrotic syndrome is kidney disease with proteinuria, hypoalbuminemia and edema.

• Nephrotic range proteinuria is 3 grams/day or more

• On single spot urine collection, it is 2 g of protein per gram of urine creatinine

etiology

• Common primary causes of nephrotic syndrome include kidney disease such as:– Minimal-change nephropaty– Menbranous nephropathy– Focal glomerulosclerosis

Con’t

• Secondary causes include systemic disease such as:– Diabetes mellitus– Lupus erythematous– Amyloidosis– Congenital and hereditary focal glomerulosclerosis – Drugs abuse such as heroin– Medication can cause nephrotic syndrome : NSAID

(MCN) and administration of older drugs of rheumatic (MN)

• Nephrotic range proteinuria could occur with the use of Anticancer agent such as bevacizumab that inhibit vasculat endothelial growth factor (VEGF)

• NRP occuring in the 3rd trimester of pregnancy is the clasical finding of preeclampsia, hypertension develops as well

epidemiology

• United states statisticsDiabetic nephropathy with nephrotic syndrome

is most common, at an estimated rate of at least 50 case/ million population

In children, nephrotic syndrome may occur at a rate of 20 cases per million children

Race-, sex-, and age related demographics

• Because diabetes is major cause of nephrotic syndrome, american indians, hispanic, and african amaerican have higher incidence of NS tha white persons

• HIV nephropathy as complication of HIV infection is unusual in whites; it is seen greater frequency in african american

• Focal glomerulosclerosis appears to be overrepresented in african american children than white children

• Male predominance in the occurance of nephrotic syndrome

• However, lupus nephritis affects mostly women

pathogenesis

• An increase in glomerular permeability leads to albuminuria and eventually to hypoalbuminemia.

• Hypoalbuminemia lowers the plasma colloid osmotic pressure, causing greater transcapillary filtration of water throughout the body and thus the development of edema

• With high capillary hydrostatic pressure or a low intravascular oncotic pressure, edema occurs

Metabolic consequences of proteinuria

• Infection • Hyperlipidemia and atherosclerosis• Hypocalcemia and bone abnromalities• Hypercoagulability• Hypovolemia• Hypertension (related to fluid retention and reduced

kidney funtion)• Malnutrition ( anorexia, infectious complication,

edema of the gut cause defective absorption) -> failure to thrive

infection

• Urinary immunoglobulin losses• Edema fluid acting as a culture medium• Protein deficiency• Immunosuppressive therapy• Decreased perfusion of the spleen

hyperlipidemia

• Related with hypoproteinemia and low serum oncotic pressure of nephrotic syndrome which then leads to reactive hepatic protein synthesis, including lipoprotein

• Elevated lipoprotein are filtered at the glomerulus leading to lipiduria

hypocalcemia

• It’s not a true hypocalcemia, but caused by low serum albumin level.

• Low bone density and abnormal bone caused by urinary losses of vitamin D and reduced intestinal calcium absorption

• But it is possible that long duration of either nephrotic syndrome or treatments (prednisone) are the important risk factor for bone disease

hypercoagulability

• Venous thrombosis and pulmonary embolism are complications of the NS.

• This can appear from urinary loss of antikoagulant proteins, such as :– Antithrombin III– PlasminogenAlong with the simultaneous increase in clotting

factors : factors I, VII, VIII and XVTE at NS 10 times higher than normal people

Permeabilitas glomerulus meningkat

LIPIDURIA

HIPERLIPOPROTEINEMIA

Kenaikan sintesa protein di hepar

Penurunan volume intra vaskular

Retensi Natrium dan air

Kenaikan volume cairan interstisial

ALBUMINURIA

HIPOALBUMINEMIA

oedem

Malnutrisi dan protein losing enteropathy

Kenaikan filtrasi plasma protein (albumin)

Kebocoran protein bound hormone/ Kalsium

Penurunan Ca plasama dan T4

Kenaikan reabsorpsi plasma protein

Katabolisme albumin dalam sel tubulus

Kerusakan sel tubulus menyebabkan aminoasiduria

↑renin-angiotensin

↑ aktivasi aldosteron

↑ resorpsi Na dalam tubular

↓NATRIURESIS

↑Volume cairan ekstra selular

Sembap/oedem

Factor Humoral

↑aktivasi simpatetik dan katekolamin

↑tahanan vascular ginjal

↓desakan starling dan kapiler peritubular

↑LFG

SINDROM NEFROTIK

Proteinuria masif

hipoalbuminemia

↓tekanan onkotik kapiler

VDE ↓