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Biomedical subjects

B K Mookerjee

Publications and source records attributed to B K Mookerjee.

54 records · Page 3Linked to original sources

Histology of human tubulo-interstitial nephritis associated with antibodies to renal basement membranes.

Twenty-seven patients with diffuse "crescentic" glomerulonephritis (CSGN) were identified in 1,174 renal biopsies from nephritic patients. Patients were assigned to three groups on the basis of the immunofluorescent study of renal biopsy specimens and serologic findings. Group I included eight patients with antibodies to glomerular (anti-GBM) and tubular (anti-TBM) basement membranes; group II had eight patients with only anti-GBM antibodies; and group III had eleven patients with CSGN unassociated with antibodies to either GBM or TBM. Patients with anti-GBM/anti-TBM antibodies (group I) had severe tubulointerstitial (TI) nephritis, as characterized by the infiltration of polymorphonuclear leukocytes and macrophages along the TBM and peritubular vessels. In some patients, focal proliferation of epithelial cells of proximal convoluted tubules (PCT), gaps or extensive destruction of TBM, lesions in the walls of small peritubular vessels, and interstitial giant cells were also observed. Patients with anti-GBM antibodies (group II) had mild to moderate interstitial cellular infiltration and mild tubular changes. Five patients with CSGN not associated with antibodies to renal basement membranes (group III) had mild to moderate interstitial cellular infiltration and tubular changes. A sixth patient, with Wegener's disease had severe granulomatous TI lesions. The results of this study show that TI nephritis is most frequent and severe with anti-TBM antibodies are demonstrable and suggest that anti-TBM antibodies contribute to the development of TI lesions.

Adult↗

Correlation of biochemical parameters in serum and saliva in chronic azotemic patients and patients on chronic hemodialysis.

In patients who are receiving chronic hemodialysis treatments, concentrations of creatinine and uric acid in serum correlated significantly with those in simultaneously drawn unstimulated whole saliva, both before and after dialysis. Similar correlation was shown also in a group of moderately azotemic patients who had not yet entered the chronic hemodialysis program. Use of whole saliva in these tests instead of blood samples may reduce the iatrogenic component in anemia, the frequency of venipunctures and of blood samplings. This may be a boon particularly in pediatric patients and in other patients where, due to a variety of reasons, this is desirable.

Adolescent↗

Hemodialysis for phenformin associated lactic acidosis.

A patient who attempted suicide by ingesting a large amount of phenformin developed a severe lactic acidosis. After receiving hemodialysis on two successive days, she recovered without sequela. On both occasions, the dialyses temporarily improved the degree of acidosis. The amount of phenformin extracted during these two procedures was measured and found to be only 1.5% of the total amount of drug ingested. Therefore, it is felt that hemodialysis does not remove the offending drug but does play a supportive role in the management of these patients by temporarily ameliorating some of the biochemical abnormalities.

Acid-Base Imbalance↗

Endocarditis in hemodialysis patients with systemic disease.

The presence of systemic disease may further increase the risk of bacterial endocarditis in the patient on chronic hemodialysis. Three patients are described; one with primary amyloidosis, a second with insulin dependent diabetes mellitus, and a third with heroin nephropathy who developed S.B.E. While the presence of the uremic state may hinder the recognition of endocarditis, the development of transient neurologic deficits, recent access infections and recurrent bacteremic episodes should be looked for as early clues to the diagnosis in this patient population.

Adult↗

Functional characteristics of monocytes. 1. Essential role in the transformational response of human blood lymphocytes to phytomitogens.

Phagocytic glass-adherent mononuclear cells in peripheral human blood (morphologically monocytes) have been shown to play an essential role in lymphocyte transformational response to phytomitogens. Lymphocytes from peripheral blood have been exhaustively depleted of monocytes by successive treatments, first with opsonized iron particles with eventual magnetic elimination of phagocytic cells, followed by filtration of the same population through packed glass-sand columns. This subpopulation, enriched in T lymphocytes and containing around 4% B lymphocytes, does not transform in response to concanavalin A, phytohemagglutinin, or pokeweek mitogen unless viable monocytes are added to the culture. Supernatant fluids from monocyte-enriched human blood leukocyte cultures can substitute for monocytes in restoring response. Interaction of the phytomitogen with lymphocyte, while essential, is not sufficient to trigger transformation, requiring a second signal provided by the monocyte probably via release of soluble mediators.

Cell Adhesion↗

Renal prostaglandins and the regulation of blood pressure and sodium and water homeostasis.

In addition to its well known prohypertensive role in various states of experimental and human hypertension, the kidney has also been shown to exert an antihypertensive "endocrine" function. According to this hypothesis, certain forms of experimental and human hypertension might not solely be the result of an excess in the activity of such renal pressor systems as the renin-angiotensin system and the sympathetic nervous system, but might also result from an absolute or relative deficiency of intra-renal vasodilator antihypertensive factors which might allow pressor systems to act unopposed to produce peripheral arteriolar vasoconstriction and sustained hypertension. At least four factors have been characterized in the kidney of various animal species and man which might be responsible for such an antihypertensive function. These are (1) the renomedullary prostaglandins (PGs), (2) the renomedullary antihypertensive neutral lipid, (3) antirenin phospholipid and (4) the renal kinins. This review is restricted to an examination of the possibility that the vasodepressor renomedullary prostaglandins (PGA and/or PGE) may, at least in part, mediate the so-called antihypertensive function of the kidney and participate in the regulation of renal blood flow and natriuresis by physiologic antagonism of various renal vasoconstrictor stimuli such as the renal renin-angiotensin and the sympathetic nervous systems.

Animals↗

Influence of separation techniques on the distribution and function of lymphocyte subpopulations. A comparison of three techniques.

The effect, if any, of three different lymphocyte separation techniques on the composition and functional characteristics of the purified cell suspensions has been studied. Each separation technique was shown to yield a cell population with highly specific and reproducible characteristics. The Ficoll-Hypaque technique led to good lymphocyte yields but low yields of sheep erythrocyte-rosetting (E-rosetting) T cells, and the separated cell population responded least well to phytohemagglutinin. The glass sand filtration technique led to lowest overall yield of small lymphocytes and of EAC-rosetting cells. There was significantly lower total yield of E-rosetting T cell as well, but the separated lymphocyte suspension had excellent purity, had relatively high percentage of E-rosetting T cells, and they responded extremely well to phytohemagglutinin (PHA) and pokeweed mitogen (PWM). The Technicon separation involving magneticremoval of phagocytic cells by exposure to iron particles consistently led to large yields of small lymphocytes with good purity, the largest total harvests of E-rosetting T cells, as well as EAC-rosetting cells while the separated population had the highest percentage of E-rosetting cells and responded very well to PHA and PWM. These results show that lymphocyte losses during purification are not nonspecific and that the choice of the separation technique profoundly affects the characteristics of the purified lymphocyte population obtainable.

Cell Separation↗

Inhibitory effect of furosemide on glucose transport.

The carrier-mediated glucose transport function in the intact human erythrocytes and also that of their isolated membranes is markedly inhibited in the presence of furosemide in vitro. A noncompetitive process is believed to be involved since the transport inhibition was not affected by the presence of high concentrations of glucose in the medium. The inhibition developed slowly over 2 hours. Most of the inhibition was slowly reversed during a 3-hour incubation in medium free of the drug. It is concluded that furosemide inhibits the glucose transport function directly in absence of insulin-mediated transduction mechanism and independently of any interference with intracellular glycolysis.

Biological Transport, Active↗

Antagonism of the effects of furosemide by indomethacin in normal and hypertensive man.

Furosemide and the prostaglandin synthetase inhibitor, indomethacin, were administered singly and in combination to four normal subjects and six patients with essential hypertension in order to determine whether the antihypertensive, natriuretic and other effects of furosemide could be altered by inhibition of prostaglandin synthesis. In all subjects indomethacin treatment alone resulted in a significant elevation of blood pressure and a fall in plasma renin without any change in sodium excretion. Furosemide alone resulted in a significant blood pressure fall with a rise in plasma renin and urinary aldosterone with a marked increase in urinary sodium loss. These effects were either obviated or blunted by addition of indomethacin. The results are compatible with hypothesis that the antihypertensive and natriuretic effects of furosemide might be mediated at least in part by prostaglandin synthesis. In addition, the effects of indomethacin should be considered when using this drug in hypertensive patients and in subjects requiring diuretic therapy.

Aldosterone↗

Tuberous sclerosis with striking renal involvement in a family.

We describe five cases of tuberous sclerosis in members of one family, all having renal involvement but with differences in age of onset and mode of presentation. Clinical, laboratory, and pathologic features helpful in diagnosing this condition and in distinguishing it from polycystic kidney disease and renal neoplasms are stressed. Tuberous sclerosis should always be considered in differential diagnosis of patients with multiple cystic renal lesions, particularly when age of onset of symptoms ranges from infancy to adult life in different members of one family. Absence both of specific glomerular or tubular lesions in ultrastructure and of major abnormalities in renal tubular function supports the existing concept that replacement of nephrons by hamartomatous lesions is the cause of progressive renal failure.

Adenoma↗

Case report: mesangial IgA-IgG deposition in mixed cryoglobulinemia.

Glomerular deposits of immunoglobulin A (IgA) (and immunoglobulin G [IgG]) has been described in IgA-nephropathy (Berger's disease), in anaphylactoid purpura, and systemic lupus erythematosus. The pathogenesis of mesangial IgA deposits in these disease states is unclear. Circulating immune complexes have been speculated to be involved although their existence in blood in IgA nephropathies have never been reported. We describe a 53-year-old man who presented with a petechial rash in lower extremities accompanied by painful swelling of left ankle and wrist. Polyclonal elevation of IgA and IgG in serum was found, along with cryoglobulins containing IgA and IgG (rheumatoid factor positive). After two years, hematuria, mild proteinuria, and active urinary sediment developed and renal biopsy revealed focal proliferative changes. Immunofluorescence revealed predominantly mesangial deposits of IgA and IgG but no IgM nor complement. This experience suggests that circulating complexes consisting of IgA and IgG may lead to renal lesions presenting clinically and histologically in a way similar to that commonly seen in IgA nephropathies.

Cryoglobulins↗

Calcium uptake during mitogenic stimulation of human lymphocytes: characterization of intracellular calcium compartments and demonstration of the presence of immunoreactive calrecticulin.

Phytohemagglutinin (PHA) stimulation of human peripheral blood lymphocytes (HPBL) rapidly increases 45Ca2+ uptake into intracellular pools. Detectable increase in 45Ca2+ uptake occurred only on exposure to mitogenic lectins but not with non-mitogenic lectins. However, intracellular free Ca2+ concentration [(Ca2+)i] increased comparably on exposure to either mitogenic or non-mitogenic lectins. Permeabilization of 45Ca2+ loaded cells revealed distinct pools of Ca2+ uptake. The highly digitonin sensitive pool #I (permeabilized by 0.02% digitonin) exchanged slowly and included a part that represented endoplasmic reticulum. Pool II was defined by lower digitonin sensitivity, had a much faster initial uptake. Pool III was digitonin-resistant and predominantly non-vesicular. During the first 120 min of PHA stimulation, significant increase in 45Ca2+ uptake occurred only into pool II. Progressive increase in uptake into pool I then occurred so that by 24 hours, this pool constituted the major fraction of PHA induced increment in total 45Ca2+ uptake. Using specific antibody to the calcium binding protein calreticulin, an analogous immunoreactive protein was detectable in resting HPBL. PHA stimulation led to a striking increase in abundance of immunoreactive calreticulin so that 24 hrs after PHA stimulation, there was a 28 and 3.4 fold increase in the amount of immunoreactive calreticulin present in the non-particulate fraction and the total particulate membrane fraction, respectively. A major part (72%) of the total cellular immunoreactive calreticulin in PHA stimulated cells at 24 hrs was released into the medium after permeabilization of lymphocytes with 0.02% digitonin, corresponding to the location of calcium uptake pool I.

Autoantigens↗