Shock as a Complication of the Nephrotic Syndrome

Egan, Thomas J.; Kenny, Frederic M.; Jarrah, Azmi S.; Holliday, Malcolm A.

doi:10.1001/archpedi.1967.02090180124012

Cited by 5 publications

(4 citation statements)

References 19 publications

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“…A reduction in plasma volume is the most common explanation of the reduced GFR (14,16). Although hypovolaemia may occur in the nephrotic syndrome (17,18), it has recently been shown that this is usually not the case (2,19). Nor is the reduced GFR accompanied by a corresponding reduction in the renal plasma flow (2, 3) but instead, a low FF has been reported (2, 3) and has been suggested to be caused by a reduced glomerular permeability to water (3).…”

Section: Discussionmentioning

confidence: 99%

Clinical Course and Renal Function in Minimal Change Nephrotic Syndrome

Bohlin

1984

Acta Paediatrica

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Thirteen unselected children with the minimal change nephrotic syndrome were followed for 11 months-7.5 years, during which time 32 renal function tests were performed. Glomerular filtration rate (GFR) was determined as clearance of inulin using a standard clearance technique. The children had between zero and 34 relapses and three developed steroid resistance. Three patients had severe but reversible complications related to the corticosteroid therapy. Chlorambucil was given to four patients, of whom three with steroid resistance had lasting remissions, whereas one patient with frequent relapses had only transient improvement. The GFR was decreased at the first episode in six patients, whose clinical course did not differ from that of the others. None had a decreased GFR later in the course of the disease. It is concluded that reduced GFR at the onset of the minimal change nephrotic syndrome is reversible and does not imply an unfavourable outcome.

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Section: Discussionmentioning

confidence: 99%

Clinical Course and Renal Function in Minimal Change Nephrotic Syndrome

Bohlin

1984

Acta Paediatrica

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“…Patients, usually children, with the nephrotic syndrome who are in remission occasionally have a relapse, with profound proteinuria and loss of albumin in urine and into ISF sufficient to cause shock. The loss may reduce PV by half and plasma albumin even more [38,39]. While the first impulse is to give albumin as HSA, giving only Ringer's solution may be better.…”

Section: Isf Support When Pv Is Compromisedmentioning

confidence: 99%

Extracellular fluid and its proteins: dehydration, shock, and recovery

Holliday

1999

Pediatric Nephrology

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This review highlights characteristics of extracellular fluid (ECF) that are often overlooked. ECF has, in addition to plasma and interstitial fluid (ISF) surrounding cells, a third large compartment, the ISF of skin and connective tissue. This acts as a reservoir that gives up ECF to plasma volume (PV) in order to sustain circulation in the event of either shock or dehydration. While Starling forces drive filtration, ECF is returned to PV more by lymph and less by Starling forces than previously appreciated. Lymph return to PV is dependent on physical activity and muscle contraction to overcome gravity. Regional change in metabolic rate alters the need for oxygen and nutrients that is met by a regional increase in capillary blood flow. Blood flow is controlled by vasoactive compounds released in response to a drop in PO(2); these relax capillary smooth muscle to increase blood flow and delivery of oxygen and nutrients. Plasma proteins, including albumin, are filtered into the interstitium through larger pores than those filtering ECF. The rate of protein filtration is set by size and charge of these larger endothelial pores and by size and charge of proteins. Charge of these pores, hence albumin permeability, is regulated by many of the same vasoactive compounds that control capillary flow. As a consequence, in response to gravitational stress and other forms of shock that reduce effective circulation, albumin as well as ECF is rapidly shifted from plasma and sequestered in ISF. When this has occurred, as in burn shock, restoration is better effected by generous expansion of ECF with Ringer's solution alone, rather than with Ringer's solution supplemented with human serum albumin or other colloid. Restoring both PV and ISF volume restores lymph circulation and returns sequestered albumin to PV.

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“…In pediatric practice, the primary type appears more frequently than the secondary type. The ratio of primary to secondary type has been reported as 3:7 (Yamauchi and Hopper, 1964) but there are many reports which show all are primary type (Reimold et al 1966;Egan et al 1967;Tagawa et al 1973;Okamura et al 1982; and this study).…”

Section: Discussionmentioning

confidence: 51%

“…It had then been speculated that the cause of nephrotic crisis (Cx) was an infection such as pneumococcic bacteriemia or penitonitis. Other causes have been suggested, (Yama chi and Hopper, 1964) More recently there have been many pediatric reports of spontaneous Cx, where hypovolemic shock has been proposed as a main factor in the cause although there was little evidence reported and the role of hypoadrenocorticism was ignored, (Reimold et al 1966;Egan et al 1967;Nonoda et al 1973;Tagawa et al 1973 andOkamura et al 1982).…”

Section: Introductionmentioning

confidence: 99%

Pathogenesis of "nephrotic crisis" in children.

Yoshimoto

1984

Kurume Med. J.

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We examined 20 episodes of nephrotic crisis (Cx) in 13 nephrotic children and report hematological findings and pathogenesis of the crisis. All physical and clinical data including serum and plasma protein levels and urinalysis, were recorded at the onset of Cx, during recovery and the interventing interval. There was a total of 20 incidences of Cx: 17 occurred at relapses and 3 at the onset of the nephrotic syndrome. We compare the Cx data with the data we additionally collected from 14 other children suf f erring with nephrotic syndrome but without the complication of Cx (non-Cx) either at relapses (10) or first onset (4). The most characteristic Cx clinical manifestations (compared with non-Cx group) were abdominal pain in 85 % (cf. 14.3 %), vomiting in 70% (cf. 0 %), and facial pallor in 65% (cf. 7.1 %). There were significant differences of the Cx clinical and hematological data when compared with the non-Cx data. The Cx group showed a significantly lower blood pressure, higher hematocrit value, lower serum sodium concentration, lower C3 level, lower CH50 activity and lower serum total protein and albumin (standardized for hematocrit values). We conclude that hypovolemia was the pathogenesis for Cx: the sudden loss of massive serum protein into urine, causing subsequent hypoproteinemia (hypoalbuminemia) and decreased colloidal osmotic pressure impairing re-entry transport of interstitial fluids from tissue to the blood. The hypovolemia of Cx is aggravated by the hyponatremia which arises due to a sodium shift from the blood to interstitial tissue. We investigated the role and mechanism of a possible hypoadrenocortical state and report negative findings in all cases.

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Shock as a Complication of the Nephrotic Syndrome

Cited by 5 publications

References 19 publications

Clinical Course and Renal Function in Minimal Change Nephrotic Syndrome

Clinical Course and Renal Function in Minimal Change Nephrotic Syndrome

Extracellular fluid and its proteins: dehydration, shock, and recovery

Pathogenesis of "nephrotic crisis" in children.

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