Functional proteinuria

Produces the following symptoms when methionine is not in the diet impairment of liver function, proteinuria, hematuria, dermatitis, leucopenia, thrombocytopenia, and diarrhea. Deterioration of mental status may also occur. All symptoms are reversed or prevented by methionine.3... 

Patients receiving cytotoxic drug treatment should be evaluated for drug-related toxicities every week during the initial treatment period. After 1 month of treatment, the frequency of monitoring may be reduced. When the patient is on long-term steroid treatment, monthly visits are often required for assessment of both efficacy and toxicities. If a favorable response is obtained after a course of treatment, the patient may be evaluated every 3 to 4 months. The patient s renal function, proteinuria, urinalysis, blood pressure, lipid profile. 

Hyperlipidemia plays a role in the development of cardiovascular disease (CVD) in patients with CKD. The primary goal of treatment of dyslipidemras is to decrease the risk of atherosclerotic cardiovascular disease. A secondary goal in patients with CKD is to reduce proteinuria and decline in kidney function. Treatment of hyperlipidemia in patients with CKD has been demonstrated to slow the decline in GFRby 1.9 mL/minute per year of treatment with antihyper Epidemic agents.21... 

The answer is d. (Hardman, p 7502) The most consistent of the toxicides of ACT inhibitors is impairment of renal function, as evidenced by proteinuria. Elevations of blood urea nitrogen (BUN) and creatinine occur frequently, especially when stenosis of the renal artery or severe heart failure exists Hyperkalemia also may occur These drugs are to be used very cautiously where prior renal failure is present and in the elderly Other toxicides include persistent dry cough, neutropenia, and angioedema. Hepatic toxicity has not been reported... 

Potassium-sparing diuretics may cause hyperkalemia, especially in patients with chronic kidney disease or diabetes, and in patients receiving concurrent treatment with an ACE inhibitor, ARB, NSAID, or potassium supplement. Eplerenone has an increased risk for hyperkalemia and is contraindicated in patients with impaired renal function or type 2 diabetes with proteinuria. Spironolactone may cause gynecomastia in up to 10% of patients, but this effect occurs rarely with eplerenone. 

Other clinical parameters that should be monitored periodically include funduscopic changes on eye examination, LV hypertrophy on ECG, proteinuria, and changes in kidney function. 

Progression factors hasten decline in kidney function after initiation of kidney damage. Progression factors include glycemia in diabetics, hypertension, proteinuria, and smoking. 

A secondary goal is to reduce proteinuria and renal function decline seen with administration of statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors). 

The proteinuria and aminoaciduria, and acidosis and glucosuria where they occur, are probably caused by reversible inhibition of some functions of the renal tubule. There would appear to be no structural damage to the kidney. However, 2 children developed nephrolithiasis while being treated with a low-lactose diet (B7, C5), The time course of events, when galactose is withdrawn from and returned to the diet, suggests that some metabolite of galactose accumulates in the cells of the renal tubules and has an inhibitory effect on the reabsorption of a number of substances. 

Laboratory procedures specific to galactosemia are dealt with below, but a number of other tests are also of value. Liver function tests, though sometimes helpful, are not always informative (see above, Section 2.2). Protein is usually present in the urine in untreated cases, but this occurs in other diseases. Aminoaciduria is a very common finding in galactosemia, though Holzel (H3) states it is absent in some older children with a mild form of galactosemia aminoaciduria occurs in other diseases and is frequently accompanied by proteinuria and glucosuria. 

Undesired effects. The magnitude of the antihypertensive effect of ACE inhibitors depends on the functional state of the RAA system. When the latter has been activated by loss of electrolytes and water (resulting from treatment with diuretic drugs), cardiac failure, or renal arterial stenosis, administration of ACE inhibitors may initially cause an excessive fall in blood pressure. In renal arterial stenosis, the RAA system may be needed for maintaining renal function and ACE inhibitors may precipitate renal failure. Dry cough is a fairly frequent side effect, possibly caused by reduced inactivation of kinins in the bronchial mucosa. Rarely, disturbances of taste sensation, exanthema, neutropenia, proteinuria, and angioneurotic edema may occur. In most cases, ACE inhibitors are well tolerated and effective. Newer analogues include lisinopril, perindo-pril, ramipril, quinapril, fosinopril, benazepril, cilazapril, and trandolapril. 

Hyperkalemia The principal risk of epierenone is hyperkalemia. Hyperkalemia can cause serious, sometimes fatal arrhythmias. This risk can be minimized by patient selection, avoidance of certain concomitant treatments, dose reduction of epierenone, and monitoring. The rates of hyperkalemia increase with declining renal function. Treat patients with CHF post-MI who have serum creatinine levels greater than 2 mg/dL (males) or greater than 1.8 mg/dL (females), patients who have Ccr 50 mL/min or less, and diabetic patients with CHF post-MI, including those with proteinuria, with caution. 

Renal function impairment Proteinuria and hematuria may develop and may be a warning sign of membranous glomerulopathy, which can progress to a nephrotic syndrome. 

Heynen, J. M., Blockmans, D., Verwilghen, L. R., et al, Congenital macrothrombocytopenia, leukocyte inclusions, deafness and proteinuria Functional and electronmicroscopic observations on platelets and megakaryocytes. Br. J. Haematol. 70, 441—448 (1998). 

Adverse effects include gastrointestinal disturbances after oral use, flu-like symptoms and skin reactions, mild hypocalcaemia and after intravenous administration transient proteinuria and rarely deterioration of renal function. 

ACE inhibitors have a particularly useful role in treating patients with chronic kidney disease because they diminish proteinuria and stabilize renal function (even in the absence of lowering of blood pressure). This effect is particularly valuable in diabetes, and these drugs are now recommended in diabetes even in the absence of hypertension. These benefits probably result from improved intrarenal hemodynamics, with decreased glomerular efferent arteriolar resistance and a resulting reduction of intraglomerular capillary pressure. ACE inhibitors have also proved to be extremely useful in the treatment of heart failure, and after myocardial infarction, and there is recent evidence that ACE inhibitors reduce the incidence of diabetes in patients with high cardiovascular risk (see Chapter 13). 

Once the presence of hypertension is established, the question of whether to treat and which drugs to use must be considered. The level of blood pressure, the age of the patient, the severity of organ damage (if any) due to high blood pressure, and the presence of cardiovascular risk factors all must be considered. Assessment of renal function and the presence of proteinuria are useful in... 

Mis-localisation of annexin 2 has recently been implicated in the pathogenesis of Dent s disease. This term is now used collectively to describe what was previously four conditions that affect kidney function X-linked recessive nephrolithiasis with renal failure, X-linked recessive hypophosphatemic rickets, idiopathic low molecular weight proteinuria with hypercalciuria and nephrocalcinosis and Dent s disease. Patients with this condition present with low molecular weight proteinuria and hypercalciuria. Renal stones, nephrocalcinosis and renal failure are common late-stage developments. The condition has been attributed to abnormal acidification within endosomes of the proximal tubular cells. It is very rare and is usually caused by mutations in the voltage-dependent Cl /H+ chloride antiporter CLCN5, but occasionally in the PI4,5P2 5-phosphatase, OCRL1 (oculocerebrorenal syndrome of Lowe protein 1). 

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