Ascites renal impairment

NSAIDs can cause renal impairment, particularly in patients in whom prostaglandins are playing an important role in maintaining renal function. Such patients include those taking diuretics, the elderly and those with concurrent conditions such as congestive heart failure and ascites. Hence the combination of diuretics and NSAIDs may increase the nephrotoxicity ofNSAIDs.30. - ... 

Monitoring Periodic monitoring for toxicity, including CBC with differential and platelet counts, and liver and renal function testing is mandatory. Periodic liver biopsies may be indicated in some situations. Monitor patients at increased risk for impaired methotrexate elimination (eg, renal dysfunction, pleural effusions, ascites) more frequently (see Precautions). 

Methefrexate (Rheumatrex Dose Pack, Trexall) [Antineeplastic/ Antirheumatic (DMARDs), Immunosuppressant/ Antimetabolite] warning Administration only by experienced healthcare provider do not use in women of childbearing age unless absolutely necessary (teratogenic) impaired elimination w/ impaired renal Fxn, ascites, pleural effusion severe myelosuppression if used w/ NSAIDs hepatotox can induce lung Dz ... 

Diuretics, typically spironolactone, form the main therapy, combined with restricted salt intake. Sodium restriction is usually unnecessary where fluid retention is mild, and if marked limitation (less than 40 mmol per day intake) is imposed, may lead to impaired nutrition and is poorly accepted. Diuretic treatment often requires reinforcement with loop diuretics. Treatment can be maintained if urinary sodium excretion is at least 30 mmol per day. Removal of ascites through diuresis requires fluid transfer through the intravascular fluid compartment. If diuresis is too intense the intravascular fluid volume is reduced and hypotension causes hepatorenal failure to follow. The aim should be, through monitoring weight loss, to restrict fluid removal to 0.5 kg per day. In this way the risks of hyponatraemia, renal and hepatic impairment should be reduced. 

Hepato-renal syndrome rapid progressive (type I) with rising serum creatinine levels, or non-progressive and less severe (type II) impairment of renal function, often consequent on bacterial peritonitis, with persistent ascites responds to vasoconstrictor treatment, typically with terlipressin through constriction of splanchnic vessels and improved renal perfusion. Withdrawal of treatment does not seem to lead inevitably to recurrence. Haemodialysis may also stabilise patients. 

Patients with renal diseases leading to the nephrotic syndrome often present complex problems in volume management. These patients may exhibit fluid retention in the form of ascites or edema but have reduced plasma volume due to reduced plasma oncotic pressures. This is very often the case in patients with "minimal change" nephropathy. In these patients, diuretic use may cause further reductions in plasma volume that can impair GFR and may lead to orthostatic hypotension. Most other causes of nephrotic syndrome are associated with primary retention of salt and water by the kidney, leading to expanded plasma volume and hypertension despite the low plasma oncotic pressure. In these cases, diuretic therapy may be beneficial in controlling the volume-dependent component of hypertension. 

It is difficult to obtain an accurate measure of renal function in patients with cirrhosis. A number of studies have shown that they tend to have low serum creatinine levels. This has been explained by a reduced muscle mass in cirrhotic patients and a reduced conversion of creatine to creatinine [10]. The calculation of creatinine clearance using the Cockcroft and Gault formula is also inaccurate in predicting GFR in these patients because it uses the serum creatinine level (which may be falsely low) and body weight in the calculation, which is likely to be inflated due to the presence of ascites [12]. The measured creatinine clearance, based on urinary excretion of creatinine, should theoretically be more accurate, even in patients with reduced muscle mass or impaired creatinine synthesis. However, it has been shown that this also overestimates the GFR because of an increased fractional tubular secretion of creatinine in cirrhotic patients, particularly those with reduced GFR [10]. 

Bernard , M., Santini, C., Trevisani, R, Baraldini, M., Ligabne, A., Gasharrini, G. Renal function impairment induced hy change in posture in patients with cirrhosis and ascites. Gut 1985 26 629 -635... 

Diet The diet should be evenly balanced and in accordance with the principles of present-day dietetics it must also be tolerated by the patient. There is no special diet for viral hepatitis patients. The water and electrolyte balance is often disrupted in cases of acute viral hepatitis, possibly with the occurrence of oedemas and ascites (so-called hepatitis oedematosa) (48, 77, 131) (s. p. 297) or impaired renal function (60, 120) - as is recognizable from the diuresis which normally develops at the onset of the convalescence phase. An even balance of water and electrolytes should be maintained - this is very much supported by the patient lying flat. In the event of inadequate nutrition or malnutrition, particularly when nausea and vomiting occur, substitution measures are advisable (e.g. vitamins, glucose and electrolyte infusions). 

Impairment of cerebral functions and disturbances of the water and electrolyte balance are the two most important and most common manifestations of decompensated liver cirrhosis. They may be reliably detected at an early stage by means of daily body weight control and simple psychometric tests. A documentation sheet filled in by the patient has proved to be worthwhile latent oedemas or the onset of ascites as well as latent encephalopathy can be detected in this way and thus treated at an early stage. Longterm standing leads to a reduction of natriuresis with subsequent water retention and a deterioration of renal blood flow (like a vicious circle). This is caused by activation of the RAAS and the sympathetic nervous system. Such a dangerous situation (which can arise for example after two hours of standing at a sports event with excessive emotional participation) is often underrated, as we ourselves observed in several patients (s. p. 292) (s. fig. 15.3) (see chapter 16 )... 

When diuretics are administered at the same time, it is not absolutely necessary to adhere to strict salt restriction. We followed the recommended 6-8 g/day. Indeed, such a moderate restriction is usually observed more reliably by the patient. Reducing water intake to 1.5-2.0 1/day is also sufficient. Only a hyponatraemic condition of <130 mmol/1 requires a reduction in fluid intake to <1,000 ml/day. Determination of fractional sodium elimination (FEnJ may point to potential success even before treatment has begun with a value of >0.5%, treatment steps 1 and 2 (see above) will achieve a probable success rate of about 95%. This favourable initial situation is supported by a still sufficient spontaneous sodium excretion of >40 mmol/day. Therapy resistance must be anticipated when fractional sodium elimination is <0.1% and sodium excretion is <10 mmol/day. If treatment steps 1—4 are unsuccessful or renal function is clearly impaired initially and FENa is <0.1%, the insertion of a peritovenous shunt (PVS) should be considered. This procedure is designed to make use of the principle of ascites reinfusion for as long as possible, (s. tabs. 16.14—16.18) (s. p. 311) TIPS may also prove to be an alternative to PVS, especially when using a polytetrafluoroethylene-covered stent to prevent occlusion. (Ill) (s. fig. 16.15) (s. pp 259, 314, 362)... 

The ability of sulindac to inhibit prostaglandin synthesis and impair renal function has been confirmed in a different high-risk group, namely patients with hepatic cirrhosis and ascites [82]. We have also identified the development of profound acute kidney injury in risk prone patients who received sulindac for several days to weeks. Collectively, these studies suggest caution in accepting any NSAID as being "renal sparing". 

Quintero E,Gines P, Arroyo Vet al. Sulindac reduces the urinary excretion of prostaglandins and impairs renal function in cirrhosis with ascites. Nephron 1986 42 298-303. 

Triamterene may be u.sed alone in the treatment of mild edema associated with congestive heart failure or cirrhosis of the liver with ascites, but it should not be given to patients with impaired renal function." It is not to be used alone in the treatment of hypertension. - Its primary use is in combination with hydrochlorothiazide (or other diuretics that act at site 2 or 3) to prevent the hypokalemia associated with the latter diuretics. 

Quintero E, Gines P, Arroya V, Rimola A, Camps J, Gaya J, Guevara A, Rodamilans M, Rodes J. Sulindac reduces the urinary excretion of prostaglandins and impairs renal function in patients with cirrhosis and ascites. Nephron 1986 42 298-303. Rossert J. Drug-induced acute interstitial nephritis. Kidney Int 2001 60 804-817. 

If the patient with kidney failure also has cirrhosis or some other form of hver failure, this additional ammonia load may present a stress that cannot be adequately handled by the diseased liver. The result may be increased blood and central nervous system ammonia levels with development of encephalopathy (Fraser Arieff, 1985). Thus, patients with cirrhosis and end-stage kidney disease are at particular risk for developing encephalopathy since both conditions act synergistically to increase both blood and central nervous system ammonia. It should also be noted that plasma urea and serum creatinine do not always adequately reflect renal function in patients with severe liver disease. Recent studies suggest that many patients who have cirrhosis, ascites, and normal plasma urea and creatinine may in fact have severe renal functional impairment (Gines et al., 1988 Papadakis Arieff, 1987 Takabatake et al., 1988). In such individuals, differentiation of hepatic from uremic encephalopathy on clinical grounds may be difficult. 

Contraindications for the TACE are poor performance status (Karnofsky status <50%), nutritional impairment, neoplastic ascites, high serum bilirubin level (> 3 mg%), poor hepatic synthesis (serum albumin < 2.0 mg/dl) and renal failure (serum creatinine > 2 mg%). There should be an adequate amount of residual uninvolved liver tissue. A tumor burden of more than 50%-75% resulting in an inadequate liver function is regarded as a contraindication for performing TACE (Therasse et al. 1993 Gates et al. 1999). Likewise florid infections or myelosuppres-sion (white blood cell count < 2000/ml, elementary bodies < 100,000/pl) are classified as contraindications for TACE. 

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