Even in cases of severe unilateral hydronephrosis, the overall kidney function may remain normal since the unaffected kidney will compensate for the obstructed kidney.Urinalysis is usually performed to determine the presence of blood (which is typical for kidney stones) or signs of infection (such as a positive leukocyte esterase or nitrite). Impaired concentrating ability or elevated urine pH (distal renal tubular acidosis) are also commonly found due to tubular stress and injury. Imaging studies
Imaging studies, such as an intravenous urogram (IVU), renal ultrasonography, CT, or MRI, are also important investigations in determining the presence and/ or cause of hydronephrosis. Whilst ultrasound allows for visualisation of the ureters and kidneys (and determine the presence of hydronephrosis and / or hydroureter), an IVU is useful for assessing the anatomical location of the obstruction. Antegrade or retrograde pyelography will show similar findings to an IVU but offer a therapeutic option as well. Real-time ultrasounds and Doppler ultrasound tests in association with vascular resistance testing helps determine how a given obstruction is effecting urinary functionality in hydronephrotic patients.In determining the cause of hydronephrosis, the location of obstruction can be determined with a Whittaker (or pressure perfusion) test, wherein the collecting system of the kidney is accessed percutaneously, and the liquid is introduced at high pressure and constant rate of 10ml/min while measuring the pressure within the renal pelvis. A rise in pressure above 22 cm H2O suggests that the urinary collection system is obstructed.
This requires active folate and vitamin B12, in order to donate a methyl group. Active folate is known as 5-methyltetrahydrofolate (5-MTHF). Another pathway for the conversion of homocysteine back to methionine also exists, involving methylation with trimethylglycine (also called betaine or abbreviated to TMG) as a methyl donor. The remaining homocysteine is transsulfurated to cysteine, with vitamin B6 as the co-factor.Genetic defects in 5-MTHF reductase can consequently lead to hyperhomocysteinemia. The most common polymorphisms are known as MTHFR C677T and MTR A2756G. These polymorphisms occur in about 10% of the worlds population. Elevations of homocysteine can also occur in the rare hereditary disease homocystinuria. Diagnosis
A blood test can be performed to quantify total homocysteine concentration in the plasma, of which approximately 80% is generally protein-bound. Classification of hyperhomocysteinemia is defined with respect to serum concentration as follows:
Moderate: 15–30 nmol/mL (or μmol/L)
Intermediate: 30–100 nmol/mL
Severe: > 100 nmol/mLIf total homocysteine concentration is not found to be elevated, but clinical suspicion is still high, an oral methionine loading challenge several hours prior to quantification of homocysteine concentration may be used to increased sensitivity for marginal abnormalities of homocysteine metabolism.Fasting for 10 hours is sometimes recommended prior to measurement of homocysteine levels, but this may not be necessary for diagnostic yield. Treatment
Vitamins B6, B9, or B12 supplements (alone or combined), while they lower homocysteine level, do not change the risk of heart disease or prevent death in people who have heart disease when compared to standard care or to an inactive supplement in a clinical trial.