Overview
Hyperuricemia nephropathy is a renal disease characterized by primary or secondary hyperuricemia accompanied by deposition of uric acid (or urates) in the kidneys, causing kidney stones, obstruction, interstitial nephritis, and acute or chronic renal failure as a manifestation.
Causes
Uric acidemia nephropathy is a renal damage triggered by the supersaturation of uric acid concentration in the blood and the deposition of uric acid in the renal tissues.
Symptoms
1. Acute Uric Acid Nephropathy
It is often caused by the increase of both blood and uric acid, mostly seen in myeloproliferative diseases, chemotherapy, epileptic status, heat stroke, Lesch-Nyhan syndrome and spontaneous necrosis of multiple solid tumors, which is manifested by sudden oliguria or anuria, and a rapid increase in blood nitrogen level. Early on, there may be a history of microscopic hematuria and excretion of uric acid stones, and a uric acid/urinary creatinine >1.0 favors the diagnosis. The cause of acute renal failure is the blockage of the collecting ducts by crystals, and it is also believed that the pressure of crystals on the distal renal blood vessels increases the pressure in the glomerular arterioles and the paratubular capillaries, which is an important cause.
2.Chronic gouty nephropathy
Often due to long-term hyperuricemia, uric acid crystals deposited in the renal interstitium, causing chronic interstitial nephritis manifestations, there may be mild back pain, edema and hypertension; urine is acidic, with mild to moderate proteinuria, partially accompanied by pus or bacteriuria, with stones often have hematuria; early urinary concentration and dilution of the function or the phenol red excretion rate decreases, and in the late stage due to the majority of the glomerular involvement azotemia or even uremia. However, in recent years, whether this disease is an independent disease is controversial, tends to simple hyperuricemia does not deteriorate the role of renal function, renal decompensation and patients with hypertension, atherosclerosis, coronary artery disease, diabetes mellitus, pre-existing renal disease and a history of lead exposure.
3.Uric acid nephrolithiasis
The incidence of nephrolithiasis in primary or secondary hyperuricemia is 22% and 42% respectively. Small stones can be asymptomatic, only sandy caviar-like stones in the urine; larger yellow-brown stones, depending on the size can cause urinary tract obstruction or renal colic. Uric acid stones are radiographically negative. Hyperuricemia often has extra-renal manifestations such as arthropathy, cardiovascular lesions, gout stones and gouty attacks.
Examination
1. Urine examination
Gouty nephropathy patients with urinary changes are mainly mild proteinuria and a small amount of red blood cell urine excretion, the analysis of the composition of the stones can determine whether the urate, but the technical requirements, should pay attention to blood and urine uric acid determination.
2. Blood test
Early changes in renal function is a decrease in the concentration function followed by a gradual impact on glomerular filtration function. Blood urea nitrogen, creatinine rise, but serum uric acid rise than urea nitrogen and creatinine significant, blood uric acid / blood creatinine> 2.5.
3. Other auxiliary examinations
(1) Two kinds of urate crystals can be seen under the light microscope: uric acid crystals are amorphous substances, appearing in the interstitium and tubular lumen; needle-shaped crystals of uric acid monohydroxide-water compounds appear in the renal medulla.
(2) Renal imaging: if urinary tract obstruction causes pyelonephrosis and ureteral dilatation, reflux nephropathy or obstructive nephropathy accompanied by infection, CT scan and nuclide renal scan may show bilateral kidney of unequal size, irregular shape of the kidney, and dilated or blunted calyces.
(3) Ultrasound: It shows unequal renal lesions bilaterally and helps to localize and diagnose the stones.
Diagnosis
Diagnostic criteria:
Middle-aged or older patients with renal disease manifestations including hematuria, proteinuria, edema, hypertension, and renal function impairment. Accompanied by arthralgia and urinary stones, blood uric acid is higher than 390 μmol/L, increased blood uric acid excretion is higher than 4.17 μmol/L, uroliths are uric acid components, and secondary hyperuricemia nephropathy due to other causes is excluded.
Treatment
Including low purine diet, prohibit alcohol abuse, application of drugs to inhibit uric acid synthesis (such as allopurinol), alkalinization of urine to pH 6.2 ~ 6.5 (excessive alkalinization is easy to form calcium phosphate or calcium carbonate stones), drink a lot of water to keep the daily urine output of more than 2,000 ml, and avoid the use of drugs that cause blood uric acid increase (such as loop diuretics, etc.). Although probenecid can increase the excretion of uric acid, but the increase in uric acid is not favorable to the kidneys. The extra-renal manifestations of hyperuricemia should also be actively treated, and the control of hypertension and prevention of infection are important for the protection of renal function.