The truth on current peritoneal dialysis: state of the art.

The share of peritoneal dialysis (PD) in the spectrum of chronic dialysis has decreased markedly in the Netherlands in the last 15 years. Consequently, the knowledge of nephrologists and nursing staff on PD has declined leading to a negative spiral in which loss of experience resulted in loss of enthusiasm to offer PD to patients and also in less interest in the new PD developments. All these changes took place while the results of PD improved and patient survival was at least similar to that on haemodialysis. The aim of this review is first to give a summary of the principles and practice of patient and staff education and to describe the role of the medical contribution in decision-making. On this basis, the second aim is to update internist-nephrologists on a number of issues that have been underexposed in the past. Recent patient and technique survival data of PD patients is reviewed, and also the new insights into dialysis adequacy. The presence of residual renal function is the main determinant of patient survival together with prevention of overhydration. Urea and creatinine removal are not important at all when patients are still passing urine. Many early problems with PD are due to the peritoneal catheter and suggestions are made for improvement of its function. The prevention and management of infections is reviewed, and also the regular assessment of peritoneal function. Free water transport is a predictor of encapsulating peritoneal sclerosis (EPS), which should be assessed regularly. The pathogenesis of EPS, treatment and the decreasing incidence are discussed.

Acute reactions to polysulfone/polyethersulfone dialysers: literature review and management.

Acute dialyser reactions in patients treated by haemodialysis are uncommon. We present two cases of such reactions, both in patients using a polysulfone, steam-sterilised dialyser. Patient 1 suffered from recurrent attacks of acute dyspnoea, hypoxia and hypotension that occurred early in dialysis sessions, whereas patient 2 presented with unexplained episodes of severe hypotension and vomiting in the initial phases of dialysis. After switching to a cellulose triacetate dialyser, both patients became asymptomatic during all subsequent dialysis sessions, but intentional (patient 1) and accidental (patient 2) rechallenge with the polysulfone dialyser induced an immediate recurrence of the symptoms. A literature search yielded 30 additional cases that have been reported since the turn of the century. All dialysers that provoked acute reactions contained membranes belonging to the polyarylsulfone family (polysulfone/polyethersulfone, PSu/PESu). Manifestations, usually occurring within the first 30 minutes of dialysis, included dyspnoea (69%), hypotension (66%), hypoxia (44%), bronchospasm (25%), chest pain (22%), pruritus and/or urticaria (22%) and abdominal symptoms (22%). Of the 32 patients, 14 were switched to a different PSu/PESu containing dialyser, which resulted in cross-reactivity in 12 of them (~85%). They could be treated safely with dialysers containing substituted cellulose (n = 8) or polyacrylonitrile (n = 4). Sixteen patients were successfully switched directly to a dialyser containing substituted cellulose (n = 11), polymethylmethacrylate (n = 4) or polyacrylonitrile (n = 1). Two patients were lost to follow-up. As rechallenges may be harmful, patients with acute reactions to PSu/PESu membranes should not be further tested in a trial-and-error fashion with similar membranes, but be switched directly to a non-PSu/PESu dialyser.

Management of encapsulating peritoneal sclerosis: a guideline on optimal and uniform treatment.

Encapsulating peritoneal sclerosis (EPS) represents a rare complication of long-term peritoneal dialysis (PD). It is characterised by diffuse peritoneal membrane fibrosis, progressive intestinal encapsulation and the clinical spectrum of intestinal obstruction. The pathogenesis is as yet not well understood but includes inflammation, angiogenesis and fibrosis. The current diagnosis of EPS lacks specificity and relies on clinical, radiographic or macroscopic evaluation. There is no general agreement on managing EPS although accumulating clinical data suggest drug treatment (steroids, tamoxifen), surgery (enterolysis) or a combination of both. Here, we provide a short overview on the current knowledge of EPS, with a focus on treatment. Moreover, we present a diagnostic and a therapeutic algorithm for EPS based on the best available published data and our combined experience.

Patients' representations of their end-stage renal disease: relation with mortality.

BACKGROUND: Self-regulation theory explains how patients' illness perceptions influence self-management behaviour (e.g. via adherence to treatment). Following these assumptions, we explored whether illness perceptions of ESRD-patients are related to mortality rates. METHODS: Illness perceptions of 182 patients participating in the NECOSAD-2 study in the period between December 2004 and June 2005 were assessed. Cox proportional hazard models were used to estimate whether subsequent all-cause mortality could be attributed to illness perception dimensions. RESULTS: One-third of the participants had died at the end of the follow-up. Mortality rates were higher among patients who believed that their treatment was less effective in controlling their disease (perceived treatment control; RR = 0.71, P = 0.028). This effect remained stable after adjusting for sociodemographic and clinical variables (RR = 0.65, P = 0.015). CONCLUSIONS: If we consider risk factors for mortality, we tend to rely on clinical parameters rather than on patients' representations of their illness. Nevertheless, results from the current exploration may suggest that addressing patients' personal beliefs regarding the effectiveness of treatment can provide a powerful tool for predicting and perhaps even enhancing survival.

[Polyuria and polydipsia due to renal diabetes insipidus during the use of lithium]. / Polyurie en polydipsie door renale diabetes insipidus bij gebruik van lithium.

Polyuria, thirst and polydipsia due to renal diabetes insipidus (RDI) are common side effects of long-term lithium treatment. In a man aged 56 years, the polyuria could be reduced considerably by diuretics. However, as shown in the case of a 49-year-old man, such treatment carries the risk of acute lithium intoxication due to volume depletion and reduced renal lithium clearance. A reduction in the dose of lithium prior to diuretic treatment is therefore mandatory. Although polyuria and polydipsia are generally mainly a nuisance, the condition may become life-threatening when free access to fluids is impossible. This is demonstrated by the case of a 46-year-old man who was on chronic lithium treatment with probable RDI and who developed fatal severe dehydration and hypernatraemia after traumatic brain injury. Awareness of the possibility of RDI in patients on chronic lithium treatment is therefore important.

[Chronic renal function disorders during lithium use]. / Chronische nierfunctiestoornissen bij lithiumgebruik.

Lithium is used for the treatment and prevention of bipolar disease and unipolar depression. A well-recognized adverse effect is renal diabetes insipidus resulting in polyuria and polydipsia. A debate has been going on for decades as to whether the long-term use of lithium may also cause slowly progressive renal failure. According to the literature, some decrease in renal function occurs in approximately 20% of the patients on long-term lithium treatment. Progressive renal failure probably develops in only a minority of them, but there is an increasing number of reports on patients that have become dependent upon dialysis due to the long-term use of lithium. In patients developing progressive renal failure, discontinuation of the use of lithium will have to be considered at some point in time. Limited data in the literature suggest that discontinuation of lithium may be advisable at a serum-creatinine concentration of approximately 200 micromol/l or a creatinine clearance of about 40 ml/min. The relatively large group of patients that develop less severe, nonprogressive renal failure and that continue to use lithium also deserves attention. According to the recent literature, chronic renal failure is a separate risk factor for cardiovascular disease. Adequate detection and management of hypertension, dyslipidaemia and perhaps also proteinuria may be of great importance for this group ofpatients.

Primary hyperaldosteronism, a mediator of progressive renal disease in cats.

In recent years, there has been renewed interest in primary hyperaldosteronism, particularly because of its possible role in the progression of kidney disease. While most studies have concerned humans and experimental animal models, we here report on the occurrence of a spontaneous form of (non-tumorous) primary hyperaldosteronism in cats. At presentation, the main physical features of 11 elderly cats were hypokalemic paroxysmal flaccid paresis and loss of vision due to retinal detachment with hemorrhages. Primary hyperaldosteronism was diagnosed on the basis of plasma concentrations of aldosterone (PAC) and plasma renin activity (PRA), and the calculation of the PAC:PRA ratio. In all animals, PACs were at the upper end or higher than the reference range. The PRAs were at the lower end of the reference range, and the PAC:PRA ratios exceeded the reference range. Diagnostic imaging by ultrasonography and computed tomography revealed no or only very minor changes in the adrenals compatible with nodular hyperplasia. Adrenal gland histopathology revealed extensive micronodular hyperplasia extending from zona glomerulosa into the zona fasciculata and reticularis. In three cats, plasma urea and creatinine concentrations were normal when hyperaldosteronism was diagnosed but thereafter increased to above the upper limit of the respective reference range. In the other eight cats, urea and creatinine concentrations were raised at first examination and gradually further increased. Even in end-stage renal insufficiency, there was a tendency to hypophosphatemia rather than to hyperphosphatemia. The histopathological changes in the kidneys mimicked those of humans with hyperaldosteronism: hyaline arteriolar sclerosis, glomerular sclerosis, tubular atrophy and interstitial fibrosis. The non-tumorous form of primary hyperaldosteronism in cats has many similarities with "idiopathic" primary hyperaldosteronism in humans. The condition is associated with progressive renal disease, which may in part be due to the often incompletely suppressed plasma renin activity.

Plasma aldosterone concentrations and plasma renin activity in healthy dogs and dogs with hyperadrenocorticism.

The mean (se) basal plasma aldosterone concentrations were significantly lower in 31 dogs with pituitary-dependent hyperadrenocorticism (PDH) (75 [9] pmol/litre) than in 12 healthy dogs (118 [14] pmol/litre), whereas in five dogs with hyperadrenocorticism due to an adrenocortical tumour they were significantly higher (205 [109] pmol/litre). The mean basal renin activity was not significantly different between the dogs with PDH (303 [48] fmol/litre/second), the dogs with an adrenocortical tumour (141 [63] fmol/litre/second), and the control dogs (201 [25] fmol/litre/second). At three and four hours after the intravenous administration of 0.1 mg/kg dexamethasone, the concentrations of aldosterone decreased significantly to about 60 per cent of their initial values in the control dogs but did not change in the dogs with PDH or an adrenocortical tumour. In the dogs with PDH the renin activity increased significantly after the administration of dexamethasone.

Aldosteronoma in a dog with polyuria as the leading symptom.

In a 10-year-old castrated male shorthaired German pointer polyuria was associated with slight hypokalemia, hypophosphatemia and alkalosis, as well as elevated plasma concentrations of a glucocorticoid-inducible iso-enzyme of alkaline phosphatase. Repeated measurements of urinary corticoids and normal suppressibility of the hypothalamus-pituitary-adrenocorticial axis excluded glucocorticoid excess. Urine osmolality (Uosm) did not increase during administration of the vasopressin analogue desmopressin. At the time water deprivation had caused Uosm to rise from 300 to 788 mOsm/kg, there was also plasma hypertonicity. During hypertonic saline infusion the osmotic threshold for vasopressin release was increased. The combination of elevated plasma aldosterone concentrations and unmeasurably low plasma renin activity pointed to primary hyperaldosteronism. As initially computed tomography (CT) did not reveal an adrenocortical lesion, the dog was treated with the aldosterone antagonist spironolactone. This caused Uosm to rise in a dose-dependent manner. However, well-concentrated urine was only achieved with doses that gave rise to adverse effects. Once repeated CT, using 2-mm-thick slices, had revealed a small nodule in the cranial pole of the left adrenal, unilateral adrenalectomy was performed which resolved the polyuria completely. Also the plasma concentrations of kalium, aldosterone and renin activity returned to within their respective reference ranges. The adrenocortical nodule had the histological characteristics of an aldosteronoma, with the non-affected zona glomerulosa being atrophic.In this dog with primary hyperaldosteronism the polyuria was characterized by vasopressin resistance and increased osmotic threshold of vasopressin release, similar to the polyuria of glucocorticoid excess. The possibility is discussed that the polyuria of glucocorticoid excess is actually a mineralocorticoid effect.

Hyperaldosteronism in a cat with metastasised adrenocortical tumour.

In a 12-year-old male shorthaired cat with attacks of hypokalaemic muscular weakness in spite of oral potassium supplementation, highly elevated plasma aldosterone concentrations in combination with low plasma renin activity pointed to primary hyperaldosteronism. Ultrasonography and computed tomography revealed a large left-sided adrenal tumour growing into the phrenicoabdominal vein and the caudal vena cava. The tumour and its intravascular extension were surgically removed, but the subsequent stenosis of the caudal vena cava caused congestion and renal failure. At autopsy pulmonary micrometastases of the aldosteronoma were found.

Acute aluminum encephalopathy in a dialysis center caused by a cement mortar water distribution pipe.

BACKGROUND: In Curaçao, distilled seawater from the water plant was used without further purification for hemodialysis for several decades. A new distribution pipe supplying water to a dialysis center on the island was installed in May 1996. To protect it from corrosion, this pipe was lined on the inside with a cement mortar. Because of the aggressiveness of the distilled water, calcium and aluminum (Al) leached from the cement mortar into the water used to prepare dialysate. This caused a possible hard water syndrome and definite acute Al intoxication. METHODS: We reviewed clinical details and outcome at follow-up, and arranged laboratory and toxicological studies of serum and hemodialysis water. RESULTS: Of the 27 patients who had a similar exposure ( approximately 60 hours) to the contaminated dialysate, 10 died from acute Al encephalopathy, whereas 17 patients had no or only minor symptoms and survived. The nonsurvivors were older (64 +/- 3 years vs. 52 +/- 2 years, P < 0.01) and had a lower body weight (57.5 +/- 5.9 kg vs. 86.5 +/- 4.1 kg, P < 0.01) and lower serum albumin concentrations (33 +/- 1 vs. 36 +/- 1 g/L, P < 0.01). Anuria tended to be more common in the nonsurvivors (8 out of 10 vs. 8 out of 17, P> 0.05). Serum Al concentrations, available in seven nonsurvivors, were significantly higher than in the survivors (808 +/- 127 vs. 255 +/- 25 microg/L, P < 0.01). CONCLUSIONS: The water distribution pipe was lined with a cement mortar that was probably inappropriate for transporting drinking water. Water distribution facilities as well as the dialysis community should be aware of the possibility of Al leaching from cemented water distribution pipes. Similar Al loads appear to induce a more severe intoxication in malnourished, older patients with smaller Al distribution volumes and anuria.

Hemodynamic patterns and spectral analysis of heart rate variability during dialysis hypotension.

Intradialytic hypotension, a major source of morbidity during hemodialysis and ultrafiltration, is often accompanied by paradoxical bradycardia. Relatively little is known about the sequential changes in autonomic nervous system activity up to and during the hypotensive episode. Continuous, beat-to-beat measurements of BP and heart rate were made during hemodialysis in patients prone (n = 8) and not prone (n = 11) to develop intradialytic hypotension. Off-line spectral analysis of heart rate variability (HRV) was performed to assess changes in autonomic nervous system activity during dialysis sessions both with and without hypotension. The low frequency (LF) component of HRV is thought to correlate with sympathetic nervous system activity, the high frequency (HF) component with that of the parasympathetic nervous system. In the sessions not complicated by symptomatic hypotension (n = 26), mean arterial BP (MAP) hardly fell, whereas heart rate increased from 77 +/- 2 to 89 +/- 5 bpm (P < 0.05). The LF component of HRV increased from 45.2 +/- 5.0 normalized units (nu) to 59.9 +/- 4.9 nu (P < 0.05), whereas the HF component fell from 54.8 +/- 5.0 to 40.2 +/- 4.4 nu (P < 0.05). These changes agree with compensatory baroreflex-mediated activation of the sympathetic nervous system (and suppressed parasympathetic activity) during ultrafiltration-induced intravascular volume depletion. In the sessions complicated by severe symptomatic hypotension (n = 22), the changes in heart rate and the results of spectral analysis of HRV were similar to those reported above up to the moment of sudden symptomatic (nausea, vomiting, dizziness, cramps) hypotension, whereas MAP had already fallen gradually from 94 +/- 3 to 85 +/- 3 mmHg (P < 0.05). The sudden further reduction in MAP (to 55 +/- 2 mmHg, P < 0.02) was invariably accompanied by bradycardia (heart rate directly before hypotension 90 +/- 2 bpm, during hypotension 69 +/- 3 bpm, P < 0.002). The LF component of HRV fell from 62.8 +/- 4.6 nu directly before to 40.0 +/- 3.7 nu (P < 0.05) during hypotension, whereas the HF component increased from 37.9 +/- 4.7 to 60.3 +/- 3.7 nu (P < 0.05). These findings agree with activation of the cardiodepressor reflex, involving decreased sympathetic and increased parasympathetic nervous system activity, respectively. These findings indicate that activation of the sympatho-inhibitory cardiodepressor reflex (Bezold-Jarisch reflex), which is a physiologic response to a critical reduction in intravascular volume and cardiac filling, is the cause of sudden intradialytic hypotension.

Causes of edema in the intensive care unit.

Patients in emergencies necessitating treatment in the intensive care unit (ICU) often develop generalized gross edema. The usual scenario is that in the emergency situation characterized by hypotension and (impending) organ failure, large amounts of fluids are administered that subsequently cannot be excreted adequately, even if the emergency situation subsides to a more stable condition. Three main factors underlie the inadequate restoration of volume balance: (1) impaired edema mobilization, due to the negative influence on lymphatic flow of reduced muscle activity and increased central venous pressure by mechanical ventilation; (2) secondary renal sodium retention by circulatory impairment and hypotension caused by mechanical ventilation and by the cardiodepressant and vasodilatory effects of (endo-)toxemia; and (3) primary renal sodium retention by renal vasoconstriction and filtration impediment, due to a complex of systemic and intrarenal vasomodulator activation and intrarenal endothelitis, or acute renal failure. Edema itself, as far as impeding organ function and necessitating mechanical ventilation, may further perpetuate this difficult to handle and vicious circle.

Effects of reduced renal perfusion pressure and acute volume expansion on proximal tubule and whole kidney angiotensin II content in the rat.

In previous studies high luminal concentrations of angiotensin II (Ang II) were found in rat proximal tubules. The physiological role of intraluminal Ang II remains to be established. In the present study, we investigated whether the luminal angiotensin II concentration in the proximal tubules ([Ang II]prox) can be modulated. Micropuncture studies were performed in control rats (C, N = 8) and rats subjected to acute volume expansion (VE, N = 8) or reduced renal perfusion pressure (RRP, N = 7). Changes in [Ang II]prox were compared to changes in whole kidney Ang II content ([ANG II]kidney) and the plasma concentration ([Ang II] plasma). In C rats, [Ang II]prox was 460 +/- 48 pmol/liter (10 to 20 times lower than hitherto reported), while [Ang II]kidney and [Ang II]plasma were 369 +/- 81 pmol/kg and 90 +/- 29 pmol/liter, respectively. In agreement with previous data, VE failed to suppress [Ang II]prox (674 +/- 132 pmol/liter), while at the same time [Ang II]kidney (42 +/- 10 pmol/kg) and [Ang II]plasma (12 +/- 3 pmol/liter) were markedly suppressed. This points to dissociated regulation of [Ang II] in the renal luminal compartment on the one hand and the extraluminal renal and systemic plasma compartments on the other hand. During RRP, [Ang II]prox increased significantly to 1675 +/- 465 pmol/liter. No dissociation between the three compartments was observed in this situation, as [Ang II]kidney (969 +/- 85 pmol/kg) and [Ang II]plasma (245 +/- 72 pmol/liter) increased in parallel. In summary, we confirm that Ang II is present in proximal tubules of rat kidneys at concentrations which exceed those in plasma. Its concentration could be modulated (approximately 3.5 increase) by reduction of renal perfusion pressure but not by acute volume expansion. In the latter condition, we observed a clear dissociation from Ang II generation in the extraluminal renal compartment, as whole kidney Ang II content was markedly suppressed.

Contrast-enhanced dynamic magnetic resonance imaging of the rat kidney.

This study was designed to assess whether contrast-enhanced dynamic 1H magnetic resonance imaging (DMRI) can be used to detect the effects of the loop diuretic furosemide and the vasoactive peptide angiotensin II on tubular water reabsorption in the rat kidney. A bolus of gadolinium-DTPA-dimeglumine (Gd-DTPA) (0.025 or 0.1 mmol/kg) was used as a contrast agent. The signal intensity in the magnetic resonance images relative to the precontrast signal intensity (RSI) was assessed as a function of time in the cortex and medulla. In the cortex, no differences were observed between high and low bolus injection, and between different treatment groups and controls. In the medulla, RSI patterns were different between high and low bolus, with the high bolus showing lower RSI values, because of T2 shortening at high Gd-DTPA concentrations. No difference was observed between controls and angiotensin II-infused animals. This is in line with the finding that angiotensin II did not alter medullary water reabsorption, as evidenced by unchanged urine flow and osmolality compared with controls. Medullary RSI patterns during furosemide infusion differed markedly from controls, in a manner suggesting that a lower concentration of Gd-DTPA was present compared with controls. This agrees with the well-known inhibiting effect of furosemide on medullary water reabsorption. It was concluded that, with the method used, small concentration differences of Gd-DTPA in the cortex resulting from small changes of plus or minus 20% in tubular water reabsorption, previously found to be present by direct micropuncture measurements, cannot be detected in rats. However, large changes in renal concentrating ability do result in different RSI patterns in the medulla.

Effects of low-dose angiotensin II infusion on loop segment reabsorption: a free-flow micropuncture study in rats.

1. Little direct information is available on the actions of angiotensin II beyond the proximal tubule. We therefore studied the effect of a mildly vasoconstrictive dose of angiotensin II on tubular handling of water, sodium (Na+) and lithium (Li+) in rats by means of free-flow micropuncture at the late proximal tubule and the early distal tubule. 2. Endogenous angiotensin II was suppressed by pretreatment with enalapril. Compared with a control group, angiotensin II increased mean arterial pressure by 15 mmHg. Glomerular filtration rate decreased from 1.32 +/- 0.05 to 1.10 +/- 0.05 ml/min, Na+ excretion from 0.43 +/- 0.09 to 0.13 +/- 0.03 mumol/min, fractional delivery of water at the late proximal tubule from 50.1 +/- 1.7 to 42.9 +/- 3.2%, fractional delivery of Na+ at the late proximal tubule from 46.5 +/- 1.3 to 39.1 +/- 3.5% and fractional delivery of water at the early distal tubule from 26.4 +/- 1.4 to 21.9 +/- 1.0% (P < 0.05 for each variable). Fractional delivery of Na+ at the early distal tubule did not change significantly. 3. Similar experiments were performed during partial aortic constriction to exclude the effects of increased perfusion pressure. The data obtained were similar, except that in this group the fractional delivery of Na+ at the early distal tubule decreased from 8.6 +/- 0.7 to 6.8 +/- 0.9% (P < 0.05). 4. The relation between late proximal tubule Na+ delivery and Na+ reabsorption between late proximal and early distal tubule was not disturbed by angiotensin II. For water, however, this relation tended to shift to a higher reabsorption rate.(ABSTRACT TRUNCATED AT 250 WORDS)