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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT  
Year : 2015  |  Volume : 26  |  Issue : 4  |  Page : 743-746
Effective ultrafiltration with acute peritoneal dialysis in a child with diuretic-resistant nephrotic edema


Department of Pediatric Disciplines, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, India

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Date of Web Publication8-Jul-2015
 

   Abstract 

Edema is a cardinal feature of the nephrotic syndrome and sometimes merits independent treatment. The use of diuretics is usually sufficient in the treatment of edema. Ultrafiltration (UF) may sometimes be needed in diuretic-resistant states. The use of UF for steroid-resistant nephrotic edema is scarce in children. We report a child with steroid-resistant nephrotic syndrome with diuretic-resistant nephrotic edema treated successfully using acute peritoneal dialysis as a means of UF.

How to cite this article:
Barman H, Sirie R, Duwarah SG. Effective ultrafiltration with acute peritoneal dialysis in a child with diuretic-resistant nephrotic edema. Saudi J Kidney Dis Transpl 2015;26:743-6

How to cite this URL:
Barman H, Sirie R, Duwarah SG. Effective ultrafiltration with acute peritoneal dialysis in a child with diuretic-resistant nephrotic edema. Saudi J Kidney Dis Transpl [serial online] 2015 [cited 2019 Nov 13];26:743-6. Available from: http://www.sjkdt.org/text.asp?2015/26/4/743/160197

   Introduction Top


Edema is a common clinical feature of nephrotic syndrome. It is often massive and leads to functional constraints and may result in respiratory embarrassment and locomotive restriction. [1] The majority of the nephrotic edema usually responds to diuretic therapy. The diuretic therapy has to be titrated to response and sequential blockade of the nephron may be needed. Occasionally, aggressive measures such as albumin infusion, ultrafiltration and head out immersion therapy may be needed. [1]

Here, we report a case of massive refractory nephrotic edema in the steroid-resistant nephrotic syndrome managed with the use of peritoneal dialysis as a means of ultrafiltration (UF).


   Case Report Top


A 5-year-old girl with steroid-resistant nephrotic syndrome was referred to our center with massive generalized edema, acute kidney injury and hypertension. The patient was treated elsewhere and she failed to achieve remission with four weeks of adequate daily steroid therapy and also oral cyclophosphamide and furosemide for two months. However, the generalized edema, hypertension and oliguria persisted till she was referred to our center. At presentation, she had cushingoid features and hypertension [blood pressure (BP) 130/90, >99 th percentile for age gender and height], weighed 27.40 kg and was 110 cm tall. She had facial and periorbital puffiness, massive bilateral pedal edema and gross ascites. However, her abdomen was non-tender on palpation; her vitals are summarized in [Figure 1]. Her laboratory investigations revealed impaired renal function with an estimated glomerular filtration rate (GFR) of 34.4 mg/1.73 2 /min. She was started on a stress dose of steroid (prednisolone 0.5 mg/kg/day single morning dose) and injectable antibiotics pending urine culture, which later grew Enterococcus species. Her blood culture was sterile and peritoneal fluid analysis was normal. An ultrasonography of the abdomen revealed gross ascites with normal-sized kidneys. Serum albumin was 1.2 g/dL. Other investigations are summarized in [Table 1].
Figure 1: Trend of heart rate, respiratory rate and mean blood pressure.

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Table 1: Trend of biochemical parameters, urine output and ultrafiltration (UF) volume.

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She was started on amlodipine for hypertension and a biopsy was planned. She was grossly edematous and was not even able to get up from the bed. It was decided that her edema required intensive therapy. She was put on no added salt diet. As there was no clinical evidence of intravascular hypovolemia, 2 mg/kg/ dose twice daily of IV furosemide was started. There was no response at all to two doses of furosemide and she passed only 12 mL of urine during the first day of therapy. Therefore, sequential nephron blockade using metolazone and furosemide was administered, but showed no response at all; total output was 18 mL on the second day and 76 mL on the subsequent day. As the edema was resistant to diuretics, the next options were albumin and UF. We decided against the use of albumin because it might result in an increased risk of pulmonary edema in renal failure states and hence UF was the obvious remaining choice.

Because of the unavailability of facilities of hemofiltration, the possibility of peritoneal dialysis as a means of UF was explored after discussion with the parents. Peritoneal dialysis was started on the 4 th day after a failed trial of sequential nephron blockade. All diuretics and antihypertensive drugs were withheld. Acute peritoneal dialysis was performed with a stiff peritoneal catheter. An approach of tidal peritoneal dialysis was adopted. Fluid infusion volume of 30 mL/kg/cycle was used with a dwell time of 30 min. A negative fluid balance of 2000 mL per day was targeted empirically. Sixty-two cycles were carried out in 84 h. The child tolerated the procedure well; there was no increase in heart rate or respiratory rate from baseline [Figure 1]. The BP normalized despite withdrawal of antihypertensive. The extremities remained warm throughout with a normal capillary refill time, and there was an increase in urine output due to recovery from the acute kidney injury.

The patient lost 8.2 kg after completion of the 62 cycles of peritoneal dialysis. Her BP was 100/80 mm Hg, urine output was better and renal function improved. The decrease in edema facilitated the renal biopsy, which revealed focal segmental glomerulosclerosis. The response to diuretic was re-stablished at the end of the peritoneal dialysis session. The patient was started on tacrolimus at an initial dose of 0.1 mg/kg/day titrated to 0.4 mg/kg/day. The decrease in edema was maintained on oral furosemide and metolazone and diuretics were slowly tapered off by the end of two weeks of tacrolimus. The patient was discharged a week later when the protein creatinine ratio was still >2 and serum albumin was 2.3 g/dL. She was followed-up in the pediatric nephrology clinic one month later when she was edema free and in partial remission.


   Discussion Top


The edema in nephrotic syndrome results from sodium retention. The primary mechanism of sodium retention has been greatly debated. [2] Control of edema is an integral part of the supportive care of nephrotic syndrome. Classically, the treatment of edema primarily targets renal sodium retention with the use of diuretics and not restoration of the oncotic pressure. [1] Albumin infusion alone to increase oncotic pressure causes negligible dieresis and potentiates the effect of furosemide when coadministered by improving its pharmacokinetics. [9] However, diuretics are usually not needed in cases of mild to moderate edema, as treatment with corticosteroid leads to diuresis because it induces remission in one to two weeks. In case of massive edema, where relief needs to be quick, or in case of steroid-resistant nephrotic syndrome, when early remission is unlikely, edema per se may merit treatment. A gradual reduction of edema is preferred using loop diuretics. The majority of patients with nephrotic edema respond to the above therapy. However, in a few cases, refractory edema may be noted. This may be due to the pharmacokinetic alteration of furosemide in the nephrotic state or due to diuretic braking. [4],[5],[6] Addition of metolazone or thiazide may overcome this hurdle and restore adequate diuresis. [6],[7] Co-administration of albumin infusion with furosemide is effective in cases of hypovolemia or severe hypoalbuminemia. The effect of albumin is transient, with most of the infusate is rapidly lost in urine, unless there is a remission of proteinuria. [8] Furthermore, albumin infusion carries the risk of aggravating hypertension and precipitating congestive heart failure in patients with significant refractory edema. [8],[9],[10] This could be especially true in the presence of renal failure, as in our case.

Extracorporeal UF has been suggested as an effective alternative therapy in the nephrotic syndrome with refractory edema. Various ways of achieving UF, such as hemodialysis, isolated UF and hemofiltration, have been explored in the adult population. [11],[12],[13] This technique is usually tolerated well because of rapid refilling of the intravascular space from the interstitium. [11],[13] Evidence of the efficacy and tolerability of such techniques in children in such a setting is scarce. The use of acute isolated UF may be too aggressive in children with nephrotic syndrome. The preferred extracorporeal UF method in such a setting is continuous venovenous hemofiltration, which is not a feasible option in most centers in our country because of its cost and lack of expertise. [1] In such a setting, UF via the peritoneum can be a viable option for the treatment of diuretic refractory nephrotic edema. The role of peritoneal UF has been extensively explored in adults with refractory congestive cardiac failure and type-2 cardio renal syndromes. [13],[14],[15] It has also been tried with success in adult nephrotic patients. [16] We reported a successful treatment of edema using peritoneal dialysis in a child with diuretic-resistant nephrotic syndrome. We speculate that restoration of effect of diuretics after the peritoneal dialysis in our case could be because of resolution of the acute kidney injury.

We conclude that peritoneal dialysis may be an effective mode to achieve UF in a child with diuretic-resistant nephrotic edema in a resource-limited setting.

 
   References Top

1.
Vasudevan A, Mantan M, Bagga A. Management of edema in nephrotic syndrome. Indian Pediatr 2004;41:787-95.  Back to cited text no. 1
    
2.
Deschênes G, Feraille E, Doucet A. Mechanisms of oedema in nephrotic syndrome: Old theories and new ideas. Nephrol Dial Transplant 2003;18:454-6.  Back to cited text no. 2
    
3.
Siddall EC, Radhakrishnan J. The pathophysiology of edema formation in the nephrotic syndrome. Kidney Int 2012;82:635-42.  Back to cited text no. 3
    
4.
Keller E, Hoppe-Seyler G, Schollmeyer P. Disposition and diuretic effect of furosemide in the nephrotic syndrome. Clin Pharmacol Ther 1982;32:442-9.  Back to cited text no. 4
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5.
González-Martín G, Bravo I, Ibarra N, Arancibia Clinical pharmacokinetics of furosemide in children with nephrotic syndrome. Int J Clin Pharmacol Ther Toxicol 1983;21:598-601.  Back to cited text no. 5
    
6.
Ellison DH. Diuretic resistance: Physiology and therapeutics. Semin Nephrol 1999;19:581-97.  Back to cited text no. 6
    
7.
Arnold WC. Efficacy of metolazone and furosemide in children with furosemide-resistant edema. Pediatrics 1984;74:872-5.  Back to cited text no. 7
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8.
Haws RM, Baum M. Efficacy of albumin and diuretic therapy in children with nephrotic syndrome. Pediatrics 1993;91:1142-6.  Back to cited text no. 8
    
9.
Dorhout Mees EJ. Does it make sense to administer albumin to the patient with nephrotic oedema? Nephrol Dial Transplant 1996; 11:1224-6.  Back to cited text no. 9
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10.
Indian Pediatric Nephrology Group, Indian Academy of Pediatrics, Bagga A, Ali U, Banerjee S, Kanitkar M, et al. Management of steroid sensitive nephrotic syndrome: Revised guidelines. Indian Pediatr 2008;45:203-14.  Back to cited text no. 10
    
11.
Fauchald P, Noddeland H, Norseth J. An evaluation of ultrafiltration as treatment of diuretic-resistant oedema in nephrotic syndrome. Acta Med Scand 1985;217:127-31.  Back to cited text no. 11
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12.
Asaba H, Bergström J, Fürst P, Shaldon S, Wiklund S. Treatment of diuretic-resistant fluid retention with ultrafiltration. Acta Med Scand 1978;204:145-9.  Back to cited text no. 12
    
13.
Marenzi G, Lauri G, Grazi M, Assanelli E, Campodonico J, Agostoni P. Circulatory response to fluid overload removal by extractorporeal ultrafiltration in refractory congestive heart failure. J Am Coll Cardiol 2001;38:963-8.  Back to cited text no. 13
    
14.
Mehrotra R, Kathuria P. Place of peritoneal dialysis in the management of treatmentresistant congestive heart failure. Kidney Int Suppl 2006;103:S67-71.  Back to cited text no. 14
    
15.
Wankowicz Z, Próchnicka A, Olszowska A, Baczynski D, Krzesinski P, Dziuk M. Extracorporeal versus peritoneal ultrafiltration in diuretic-resistant congestive heart failure - A review. Med Sci Monit 2011;17:RA271-81.  Back to cited text no. 15
    
16.
Morimoto S, Takahashi N, Kikuchi S, et al. Management of patients with recurrent nephrosis and intractable edema by intraperitoneal instillation of icodextrin solution. Perit Dial Int 2008;28:559-62.  Back to cited text no. 16
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Correspondence Address:
Himesh Barman
Department of Pediatric Disciplines, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong 793018
India
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DOI: 10.4103/1319-2442.160197

PMID: 26178548

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