PROTEINURIA

In the daily practice found 10% of cases of proteinuria in children 8-15 years of age. The problem is the link between proteinuria in renal disease or proteinuria in normalcircumstances. Proteinuria by dipstick values ​​are as follows:
(-): 10-20 mg / etc.
(+1): 50 mg / etc.
(+2): 100 mg / etc.
(+3): 300 mg / etc.
(+4): 1000-2000 mg / etc.

False negatives can occur in patients with proteinuria of dilute urine (Specific Gravity<1.005), as well as in patients where the dominant protein rather than albumin.


While false positives can occur in patients with gross hematuri, contamination ofantiseptics (chlorhexidine and benzalkonium chloride), urine pH> 7, the patient was in therapy zopyridine, urine concentration. Dipstick said to be positive if the result is> +1 withurine specific gravity <1.015. When> 1.015 it is said positive if the value dipstiknya> +2.Since the number of weaknesses in the examination of protein disptik then to calculateaccurately the required capacity of the 24-hour urine.

Amount of protein released by healthy children is 150 mg / 24 hours (0.15 g / 24 hours). More specifically <4mg/m2/jam, said abnormal when 4-40 mg/m2/jam and said nephroticwhen> 40mg/m2/jam. Calculating the ratio of protein / creatinine performed when urine capacity can not be done. This ratio is calculated by dividing the urine protein (mg / dl) andcreatinine (mg / dl) in urine are taken randomly. Ratio <0.5 in children <2tahun and values ​​<0.2 in children> 2tahun considered normal. When the ratio> 3 is called nephrotic. Ratio ofprotein / creatinine is equal to the 24-hour urine capacity.

Transient Proteinuria
10% of pediatric patients with proteinuria by dipstick examination of only 1% are shown tohave persistent proteinuria. Transient proteinuria may occur when temperature> 38.3; on the state of dehydration, exercise, cold exposure, congestive heart failure, seizures andstress. Proteinuri usually does not exceed 2 +. mechanisms of transient proteinuria is stillunknown. need evaluation in children with transient proteinuria.

Orthostatic Proteinuria
Found no protein in urine and was found lying in a state of the state stand called orthostaticproteinuri. In the orthostatic proteinuri not found hematuri, hypertension and renaldysfunction. The cause of orthostatic proteinuri unknown. Possible cause is a decrease inrenal hemodynamics, partial obstruction of the renal vein and circulating immune complexes.

Fixed Proteinuria
Diagnosis is established when fixed proteinuria proteinuri found lying down and standingon the circumstances. Fixed proteinuria may be caused by damage gromerular andtubular.

Glomerular Proteinuria

Can be caused by an increase in glomerular capillary wall permeaabilitas. Glomerular proteinuria may be worth 1g-> 30g / 24h. Glomerular proteinuria can be divided into selective (loss of molecular weight plasma proteins, including albumin) and non-selective (loss of albumin and larger molecules such as Ig G). Glomerular proteinuria is suspected when protein excretion> 1 g / 24 hours or is accompanied hematuri, hypertension and renal dysfunction. Causes of glomerular proteinuria:

• Acute post-infectious glomerulonephritis
• Focal segmental glomerulonephritis 
• Mesangial proliferative glomerulonephritis 
• Membranous nephropathy 
• Membranoproliferative glomerulonephritis 
• Lupus nephritis 
• Ig A nephropathy 
• Henoch-Schonlein purpura nephritis 
• Amyloidosis 
• Diabetic nephropathy 
• Sickle cell nephropathy 
• Alport syndrome

Tubular disease

• cystinosis
• wilson disease 
• Lowe syndrome 
• galactosemia 
• tubulointerstitial nephritis 
• heavy metal poisoning 
• ATN 
• renal dysplasia 
• polykistic kidney disease 
• reflux nephropathy

Examination must include the glomerular protein creatinine, 24-hour urine capacity, serumalbumin. In patients with a low degree proteinuri (150-1000 mg / dl) and other findings are not indicative of normal renal biopsy was performed, consider the post infectionglomerulonephritis. Indication of renal biopsy is proteinuri> 1000 mg/24 hours or hematuri,hypertension, and decreased kidney function.

NEPHROTIC SYNDROME
Nephrotic syndrome is a clinical condition with symptoms of massive proteinuria,hypoalbuminemia, edema, and hypercholesterolemia. sometimes accompanied bysymptoms of hematuria, hypertension and reduced kidney function. the incidence variesbetween 2-7 per 100,000 children, and are more common in boys than girls with a ratio of2:1. nephrotic syndrome can be divided into congenital nephrotic syndrome, nephroticsyndrome, primary and secondary nephrotic syndrome. in general the majority (80%) of primary nephrotic syndrome respond well to initial treatment with steroids, but about 50% of them will relapse again and about 10% no longer respond to steroid treatment.

Pathogenesis
increase in glomerular capillary wall permeability causes proteinuria andhypoalbuminemia. causes increased permeability is not well known.

• minimal lesions in the possibility of inducing T cell dysfunction due to the advent ofglycoprotein cytokines cause the loss of the glomerular capillary wall.
• in focal segmental glomerulosclerosis, lymfosit producing plasma factors that increase thepermeability of the glomerular capillary.
• occurrence of edema due to protein loss through urine causes hypoalbuminemia and decreased plasma onkotic pressure causes transudation of fluid from the intravascular to the interstitial. decrease in intravascular volume renal perfusion pressure led to a declineof renin angiotensin aldosterone system that is activated and stimulates tubularreabsorption of sodium. decline in intravascular volume stimulates antidiuretic hormoneand increases reabsorption of water in the ductus colektivus. due to decreased plasmaoncotic pressure causes fluid to move into the interstitial edema and there.
• hypercholesterolemi because hipoalbuminemi that stimulates hepatic protein synthesisincluding the synthesis of lipoprotein. lipid catabolism decreased due to lower lipoproteinlipase.

Diagnostic step
Anamnesis
common complaint is swelling in both eyelids, abdomen, legs, or whole body can beaccompanied by a decrease in amount of urine. Other complaints can also be found asreddish-colored urine.

Physical examination
On physical examination, can be found in the eyelid edema, leg, or the presence of ascitesand edema of the scrotum / labia. hypertension is sometimes found.

Investigation
Urinalysis was found in massive proteinuria (3 to 4), which can be accompanied byhematuria. on blood tests obtained hypoalbuminemia (<2.5 g / dl), hypercholesterolemia,and increased erythrocyte sedimentation rate, and the ratio of albumin / globulin is reversed. urea and creatinine levels are generally normal unless there is a decline inkidney function.

Medical therapy
Treatment with prednisone administered at a starting dose 60 mg/m2/hari or 2 mg / kg /day (maximum 80 mg / day) in divided doses for 4 weeks, followed by a 2/3 the initialdose (40 mg/m2 / day, maximum 60 mg / day) a single morning dose interval of a day(alternating doses) for 4-8 weeks. in case of relapse, then given prednisone 60 mg/m2 /day until a mussel (maximum 4 weeks), followed by a 2/3 the initial dose (40mg/m2 / day)is alternating for 4 weeks. in steroid-resistant nephrotic syndrome or toxic steroids,immunosuppressant drugs are given. such as cyclophosphamide 2-3 mg / kbBB / day for 8 weeks. weight is calculated based on weight without edema (weight for height atpercentile 50)
serum albumin levels of 1-2 g / dl; administered 0.5 g / kg / day; levels of albumin <1g/dlgiven 1g/kgBB/hari


Supportive
When there is edema anasarka needed bed rest. In addition to the provision of immunosuppressants, other supportive treatment is required,such as the provision of nephrotic diet and diuretics. diuretics were given if there is edemaor edema anasarka that interfere with the activity. if there is hypertension, antihypertensivedrugs can be added. administration of albumin / plasma performed on indications, such asrefractory edema or shock. psychological therapies to patients and parents is neededbecause the disease can be recurrent and is a chronic disease.

With the provision of prednisone or other immunosuppressants in the long term, it is necessary to monitor the possible occurrence of drug side effects of prednisone can lead to hypertension or other adverse effects, and cyclophosphamide can cause bone marrowdepression and other side effects. blood pressure checks should be done routinely. use ofcyclophosphamide on peripheral blood examination is required every week. in case ofhypertension prednisone was stopped and replaced with other immunosuppressants,bone marrow depression (leukocytes <3000ul) the drug was suspended and resumed again when leukocytes> 5000/ul.

Growth and development
Growth disorders can occur as a result of nephrotic syndrome, the disease itself or side effects of prednisone drug repeatedly in the long term. other than that this disease is acondition imunokompromais thus highly susceptible to infection. Repeated infections caninterfere with development of the patient.