scholarly journals Mechanisms of Glomerular Albumin Filtration and Tubular Reabsorption

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Akihiro Tojo ◽  
Satoshi Kinugasa
Keyword(s):  
Early Stage ◽  
Collecting Duct ◽  
Distal Tubule ◽  
Minimal Change Nephrotic Syndrome ◽  
Minimal Change ◽  
Membrane Rupture ◽  
Filtration Barrier ◽  
Podocyte Detachment ◽  
Foot Process

Albumin is filtered through the glomerulus with a sieving coefficient of 0.00062, which results in approximately 3.3 g of albumin filtered daily in human kidneys. The proximal convoluted tubule reabsorbs 71%, the loop of Henle and distal tubule 23%, and collecting duct 3% of the glomerular filtered albumin, thus indicating that the kidney plays an important role in protein metabolism. Dysfunction of albumin reabsorption in the proximal tubules, due to reduced megalin expression, may explain the microalbuminuria in early-stage diabetes. Meanwhile, massive nonselective proteinuria is ascribed to various disorders of the glomerular filtration barrier, including podocyte detachment, glomerular basement membrane rupture, and slit diaphragm dysfunction in focal segmental glomerulosclerosis, membranous nephropathy, and other glomerulonephritis. Selective albuminuria associated with foot process effacement and tight junction-like slit alteration is observed in the patients with minimal-change nephrotic syndrome, and the albumin uptake is enhanced in the podocyte cell body, possibly mediated by albumin receptors in the low-dose puromycin model. The role of enhanced podocyte albumin transport needs to be investigated to elucidate the mechanism of the selective albuminuria in minimal-change disease.

scholarly journals Mechanism Underlying Selective Albuminuria in Minimal Change Nephrotic Syndrome

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Akihiro Tojo
Keyword(s):  
Nephrotic Syndrome ◽  
A Priori ◽  
Minimal Change Nephrotic Syndrome ◽  
Cytoplasmic Dynein ◽  
Minimal Change ◽  
Filtration Barrier ◽  
Urinary Protein Level ◽  
Foot Process ◽  
Albumin Receptor ◽  
Albumin Endocytosis

As water and solutes are filtered through the slit membrane, it is an a priori concept that a slit membrane is an essential filtration barrier for proteins, including albumin. However, in cases of minimal change nephrotic syndrome, the number of slit membranes is reduced by the foot process effacement and tight junction-like cell adhesion. Furthermore, albumin endocytosis is enhanced in the podocytes under condition of minimal change disease, and albumin is selectively transported by the albumin receptor FcRn. Suppressing the endocytosis of albumin with anti-FcRn antibody decreases the urinary protein level. The expression of motor molecules, such as cytoplasmic dynein 1 and myosin IX, is increased in the podocytes under conditions of minimal change nephrotic syndrome, suggesting the enhanced transport of vesicles containing albumin. Podocyte vesicle transport may play an important role in the pathology of selective albuminuria in cases of nephrotic syndrome.

scholarly journals Role of ‘catalytic’ iron in an animal model of minimal change nephrotic syndrome

1996 ◽  
Vol 49 (2) ◽  
pp. 370-373 ◽  
Author(s):  
Norishi Ueda ◽  
Radhakrishna Baliga ◽  
Sudhir V. Shah
Keyword(s):  
Animal Model ◽  
Nephrotic Syndrome ◽  
Minimal Change Nephrotic Syndrome ◽  
Minimal Change

scholarly journals Role of basophils in the pathogenesis of minimal change nephrotic syndrome: A literature review

2014 ◽  
Vol 8 (4) ◽  
pp. 1027-1031 ◽  
Author(s):  
QINGJUN PAN ◽  
JING WU ◽  
JINGLI TAO ◽  
YANWEN CHEN ◽  
LU LI ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Literature Review ◽  
Minimal Change Nephrotic Syndrome ◽  
Minimal Change

Novel role of Vav1-Rac1 pathway in actin cytoskeleton regulation in interleukin-13-induced minimal change-like nephropathy

2016 ◽  
Vol 130 (24) ◽  
pp. 2317-2327 ◽  
Author(s):  
Chang-Yien Chan ◽  
Kar-Hui Ng ◽  
Jinmiao Chen ◽  
Jinhua Lu ◽  
Caroline Guat-Lay Lee ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Rat Model ◽  
Minimal Change ◽  
Down Regulation ◽  
Interleukin 13 ◽  
Foot Process Effacement ◽  
Foot Process ◽  
Cytoskeleton Rearrangement

Podocyte foot process effacement and proteinuria seen in our interleukin-13 (IL-13) overexpression rat model of minimal change-like nephropathy was associated with marked down-regulation of podocyte-related genes and activation of Vav1-Rac1-induced actin cytoskeleton rearrangement in the podocytes.

Role of deep nephrons and the terminal collecting duct in a mannitol-induced diuresis

1981 ◽  
Vol 240 (5) ◽  
pp. F411-F422 ◽  
Author(s):  
J. Buerkert ◽  
D. Martin ◽  
J. Prasad ◽  
D. Trigg
Keyword(s):  
Plasma Flow ◽  
Collecting Duct ◽  
Renal Plasma Flow ◽  
Distal Tubule ◽  
Sodium Reabsorption ◽  
Water Reabsorption ◽  
Single Nephron ◽  
Papillary Collecting Duct ◽  
Reduced Water

Recollection micropuncture in Munich-Wistar rats was used to study the effects of intravenous hypertonic mannitol infusions on fluid reabsorption by surface nephrons, prior to the bend of Henle's loop of deep nephrons, and along the papillary collecting duct. During mannitol diuresis, single nephron glomerular filtration rate rose significantly in surface nephrons but fell in deep nephrons. Although mannitol increased the delivery of sodium and water to the end of the proximal tubule and to the first portion of the distal tubule of surface nephrons, water and sodium were reabsorbed between these two sites. In deep nephrons, water reabsorption prior to the bend of the loop of Henle was significantly decreased. Absolute sodium delivery to this site was reduced despite a marked decrease in fractional sodium reabsorption prior to the bend. Papillary osmolality was decreased. Renal plasma flow and inner medullary plasma flow (IMPF) increased proportionally. The reduced water extraction prior to the bend of deep nephrons and the decrease in papillary osmolality could have been partly due to a concomitant increase in IMPF and a decrease in sodium delivery to the medulla. The reabsorption of delivered sodium and water by the papillary collecting duct was reduced to a greater extent than could be expected from the increase in sodium delivery.

The role of distal tubule and collecting duct sodium reabsorption in sunitinib-induced hypertension

2018 ◽  
Vol 36 (4) ◽  
pp. 892-903 ◽  
Author(s):  
Jeannine Witte ◽  
Josephine Lampe ◽  
Anna Koenen ◽  
Ines Urbaneck ◽  
Antje Steinbach ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Distal Tubule ◽  
Sodium Reabsorption ◽  
Induced Hypertension

scholarly journals Minimal Change Disease and IgA Deposition: Separate Entities or Common Pathophysiology?

2013 ◽  
Vol 2013 ◽  
pp. 1-3
Author(s):  
Brandon S. Oberweis ◽  
Aditya Mattoo ◽  
Ming Wu ◽  
David S. Goldfarb
Keyword(s):  
Iga Nephropathy ◽  
Minimal Change Disease ◽  
Minimal Change ◽  
Dramatic Improvement ◽  
Creatinine Ratio ◽  
Urine Protein ◽  
Common Cause ◽  
History Of ◽  
Foot Process

Introduction. Minimal Change Disease (MCD) is the most common cause of nephrotic syndrome in children, while IgA nephropathy is the most common cause of glomerulonephritis worldwide. MCD is responsive to glucocorticoids, while the role of steroids in IgA nephropathy remains unclear. We describe a case of two distinct clinical and pathological findings, raising the question of whether MCD and IgA nephropathy are separate entities or if there is a common pathophysiology.Case Report. A 19-year old man with no medical history presented to the Emergency Department with a 20-day history of anasarca and frothy urine, BUN 68 mg/dL, Cr 2.3 mg/dL, urinalysis 3+ RBCs, 3+ protein, and urine protein : creatinine ratio 6.4. Renal biopsy revealed hypertrophic podocytes on light microscopy, podocyte foot process effacement on electron microscopy, and immunofluorescent mesangial staining for IgA. The patient was started on prednisone and exhibited dramatic improvement.Discussion. MCD typically has an overwhelming improvement with glucocorticoids, while the resolution of IgA nephropathy is rare. Our patient presented with MCD with the uncharacteristic finding of hematuria. Given the improvement with glucocorticoids, we raise the question of whether there is a shared pathophysiologic component of these two distinct clinical diseases that represents a clinical variant.

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