The nephrotic syndrome: pathogenesis and treatment of edema formation and secondary complications

Nephrotic syndrome is an important clinical condition affecting both children and adults. Studies suggest that the pathogenesis of edema in individual patients may occur via widely variable mechanisms, i.e., intravascular volume underfilling versus overfilling. Managing edema should therefore be directed to the underlying pathophysiology. Nephrotic syndrome is also associated with clinically important complications related to urinary loss of proteins other than albumin. This educational review focuses on the pathophysiology and management of edema and secondary complications in patients with nephrotic syndrome.     

Effect of benz(a)pyrene and constant light exposure on rat liver lysosomes and biliary excretion of lysosomal enzymes

Threefold administration of benz(a)pyrene in a dose of 20 mg/kg markedly stimulated biliary excretion of lysosomal enzymes from rat liver without signs of lysosomal damage. Constant light exposure induced changes attesting to functional activation of the lysosomal apparatus in liver cells and inhibited constitutive biliary excretion of lysosomal enzymes. Combined treatment decreased, but not abolished the stimulatory effect of benz(a)pyrene on vesicular transport of lysosomal enzymes to the bile.__________This revised version was published online in August 2005 with the addition of the issue titleTranslated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 139, No. 1, pp. 40–43, January, 2005     

Spatial synaptic distribution of recurrent and group Ia inhibitory systems in cat spinal motoneurones

1. The reversal potentials of several types of inhibitory post-synaptic potentials (IPSPs) have been studied in cat spinal motoneurones with and without modification of intracellular chloride ion (Cl(-)) concentration. Single barrel intracellular micropipette electrodes have been used.2. When studied with potassium citrate filled micropipettes, the reversal potential for IPSPs evoked by stimulation of antagonist group Ia afferents is the same as that for recurrent IPSPs evoked by antidromic stimulation of motoneurone axon collaterals, confirming earlier observations (Araki, Ito & Oscarsson, 1961; Coombs, Eccles & Fatt, 1955).3. Studied with potassium chloride filled micropipettes. the reversal potential for the group Ia IPSP was found to be different from that for the recurrent IPSP when the amount of Cl(-) diffusing or iontophoretically injected into the motoneurone was small. The amount of difference in reversal potential varied from cell to cell but when present the group Ia IPSP reversed to a depolarizing potential more readily than the recurrent IPSP in all cases.4. Interaction between recurrent IPSPs and monosynaptic excitatory post-synaptic potentials (EPSPs) was also studied and the amount of non-linearity of potential summation was measured.5. The results are consistent with the hypothesis that the terminations of Renshaw cells responsible for the recurrent IPSP are located largely on the proximal dendrites of motoneurones, while the terminations of the interneurones generating the group Ia IPSP appear to be closer to or on the cell somata.