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| IgA nephropathy |
Monitor patients with isolated hematuria without proteinuria or hypertension with urinalysis, renal function testing, and blood pressure measurement.
Treat hypertension early and aggressively. A reasonable goal is to aim for BP of 125/75-130/80mmhg.[6]
ACE inhibitors are the preferred agents for lowering blood pressure.
The decrease in proteinuria with ACE inhibitors may be an effect of decreasing the intraglomerular pressure and of changing the glomerular size selectivity.
Reports have demonstrated that ACE inhibitors are more effective than other antihypertensive drugs in slowing the progression of proteinuric renal disease.
The goal for proteinuria control is 500mg/day or less, so ACE inhibitors or ARBs should be started in patients with 24-hour urine protein of 500 mg or more.
Angiotensin II receptor blockers should be used for patients who cannot tolerate ACE inhibitors. ACE inhibitors and angiotensin II receptor blockers may have an additive effect in decreasing proteinuria. Whether high doses of ACE inhibitors better preserve renal function than combined therapy with ACE inhibitors and angiotensin II receptor blockers is unknown.
patients with advanced kidney failure.
Administer prednisone for 4-6 months to patients who have IgA nephropathy with preserved renal function, nephrotic syndrome, and minimal-change findings on light microscopy.
Manno et al, in a prospective, open-label, multicenter, centrally randomized, controlled trial, investigated whether the use of a corticosteroid in combination with an ACE inhibitor would be more effective in treating patients with IgA nephropathy than would an ACE inhibitor alone.[8] Results of the trial, in which 49 patients with IgA nephropathy were administered the ACE inhibitor ramipril and 48 patients were given ramipril plus prednisone, suggested that the combination treatment was more effective than the ACE inhibitor alone in discouraging progression of renal disease associated with IgA nephropathy.
How is IgA Nephropathy diagnosed?
Blood in the urine can be caused by many things. Because so few doctors are familiar with IgAN, a patient may be put through extensive urological tests to determine if there is a urinary tract infection or congenital abnormality. But if the red blood cells in the urine are examined under a microscope, they appear dysmorphic [strangely shaped]: instead of being full and round, they look as if they’d been nibbled around the edges. This is a tip-off that glomerulonephritis is involved, but it does not tell the doctor which glomerulonephritis it might be.
A physician may first believe that this is post-streptococcal glomerulonephritis [PSGN], a disease that resembles IgAN in some ways (but which, unlike IgAN, tends to resolve itself spontaneously). To assist the diagnosis, the doctor performs a variety of tests, including a complete blood count, blood-urea-nitrogen [BUN], serum creatinine, and ASO titers to rule out the possibility of post-streptococcal glomerulonephritis.
Your doctor may also order a creatinine clearance test. Based on a 24-hour urinalysis, this test ascertains how well they kidneys are performing their vital task of clearing creatinine, the end product of muscle metabolism, from the blood. The results show the kidneys’ glomerular filtration rate. This test is not diagnostic of a particular disease but, rather, of the severity of the inflammation and, possibly, the extend of damage to the kidneys. Your kidneys ordinarily filter about five ounces of blood each minute, but in IgAN, the filtration rate may decline because infiltration of the glomerular capillaries by inflammatory cells reduces the amount of surface area available for filtering work.
A proper diet can double the curative effect, but a bad diet may make your disease worse. So pay attention to the foods you eat, if you need any help in making the diet plan or cure your disease, you can email us. Our email: sjzkidneyhospital@hotmail.com
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