Evaluation of proteinuria
Dr PJ Mani,
It is common to see laboratory reports of albuminuria such as 1+ or trace protein in many people with apparently normal health. This can be the cause of much anxiety. How should such results be interpreted? This can be better understood if the mechanism of proteinuria is made clear. Only about 30 % of the protein excreted in normal urine (150mg) is albumin and the rest is Tamm Horsfall protein and other proteins. The testing for protein is done with simple methods like heat test which is surprisingly sensitive, but not specific for albumin . The sulphosalicylic acid test which is commonly done in hospitals is also not specific for albumin and has in addition false positivity with radiocontrast agents and cephalosporins. The dipstick stick is convenient and specific for albumin however, the results can vary as much as 1-3+ even in normal urine if it is very concentrated.
Thus quantification of urine protein is useful to determine the degree of proteinuria. 24 hour urine protein is accurate and relatively inexpensive but cumbersome. The urinary protein creatinine ratio is a good substitute for a formal 24 hour protein estimate, a ratio of more than 3 correlates well with nephritic syndrome.
Both glomerular and tubular diseases can produce pathological proteinuria , however albuminuria is commoner as tubular diseases producing proteinuria are uncommon and not likely to be very significant medically. Overflow proteinuria , due to overproduction can also occur, orthostatic protineuria in adolescents is probably due to compression of the renal vein by the superior mesenteric artery (Nut cracker kidney). Acute nephritis is one the commonest cause of proteinuria in children. Even though the incidence of post streptococcal rheumatic fever is steadily declining, the post infectious nephritis is still common in our society. The proteinuria may persist for months to years after the event but progression to renal failure is rare (less than 3%). The commonest form of nephritis world wide is actually IGA nephropathy, a disease which can present with a wide variety of presentations starting from asymptomatic haematuria and proteinuria, to synpharyngeal nephritis (i.e haematuria and proteinuria immediately following a upper respiratory infection) and chronic renal failure. This disease may be the cause of CRF presenting the the majority of Indian patients . 50% of those with malignant hypertension are also estimated to have the same disease. Several histological forms of the disease respond to treatment, the others do not. Modes of therapy include immunosupression with prednisolone, pulse methylprednisolone, mycophenolate mofetil, cyclosporin, Omega 3 fatty acid therapy (fish oil) and can prevent progression to renal failure.
Proteinuria is thus an important marker in the monitoring of disease, somewhat akin to ESR in general medicine.
Kidney - A Keyplayer in MOD
Dr. Jose P. Paul
Consultant Nephrologist, AIMS
Multiple Organ Dysfunction Syndrome (MODS) is defined as dysfunction of more than one organ requiring intervention to maintain homeostasis. Renal dysfunction in MODS is a late event and has shown an increased incidence in the last decade. The pathogenesis of ARF in MODS is multifactorial, hypotension being the main culprit. Since there is no specific therapy for established ARF, preventive measures are important.
Early volume repletion, hemodynamic resuscitation and prompt management of hypoxia constitute the cornerstone of renoprotective measures. Current studies have shown that there is no role for early dialysis, use of loop diuretics as well as renal dose of dopamine in preventing ARF.The indications for dialysis are uremia, hyperkalemia, fluid overload and metabolic acidosis. In a hemodynamically stable patient, intermittent hemodialysis is the preferred dialytic modality, while in an unstable patient, continous renal replacement therapy (CRRT) is preferred. Peritoneal dialysis is less preferred, except in children because of poor solute clearance.