Glomerular Filtration I DR.CHARUSHILA RUKADIKAR Assistant Professor Physiology GFR 1
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Relationship Between Energy Requirements for Na+Reabsorption
Kidney international, Vol. 29 (1986), pp. 32—40 Relationship between energy requirements for Na reabsorption and other renal functions JULIUS J. COHEN Department of Physiology, University of Rochester, Rochester, New York, USA In the intact organism, while the kidney is only —1% of totalkidney in that: (I) Na transport is inhibited by amiloride [7, 81 body weight, it utilizes approximately 10% of the whole bodyand (2) only a small fraction (5 to 10%) of the Na transported 02 consumption (Q-02).Becausethere is a linear relationshipfrom the mucosal to serosal side leaks back to the inucosal side between change in Na reabsorption and suprabasal renal 02[7, 81. In such a tight epithelium, net Na flux is therefore a consumption, the high suprabasal renal Q-02 has been attrib-close approximation of the unidirectional active Na flux. If no uted principally to the energy requirements for reabsorption ofother energy-requiring functions are changed when Na trans- the filtered load of Na [1—31. The basal metabolism is theport is varied, then a reasonable estimate of the energy require- energy which is required for the maintenance of the renal tissuement for both net and unidirectional active Na transport may integrity and turnover of its constituents without measurablebe obtained from measurements of the ratio, Anet T-Na5/AQ- external (net transport or net synthetic) work being done.02. However, there is now considerable evidence that there are Assuming that 3 moles of ADP are phosphorylated to form other suprabasal functions of the kidney which change inATP per atom of 02 reduced in the aerobic oxidation of I mole parallel with Na reabsorption and which require an energyof NADH by the mitochondrial electron transport chain (that is, input separate from that used for Na transport. -
Albumin in Health and Disease: Protein Metabolism and Function*
Article #2 CE An In-Depth Look: ALBUMIN IN HEALTH AND DISEASE Albumin in Health and Disease: Protein Metabolism and Function* Juliene L. Throop, VMD Marie E. Kerl, DVM, DACVIM (Small Animal Internal Medicine), DACVECC Leah A. Cohn, DVM, PhD, DACVIM (Small Animal Internal Medicine) University of Missouri-Columbia ABSTRACT: Albumin is a highly charged, 69,000 D protein with a similar amino acid sequence among many veterinary species. Albumin is the major contributor to colloid oncotic pressure and also serves as an important carrier protein. Its ability to modulate coagulation by preventing pathologic platelet aggrega- tion and augmenting antithrombin III is important in diseases that result in moderately to severely decreased serum albumin levels. Synthesis is primar- ily influenced by oncotic pressure, but inflammation, hormone status, and nutrition impact the synthetic rate as well. Albumin degradation is a poorly understood process that does not appear to be selective for older mole- cules.The clinical consequences of hypoalbuminemia reflect the varied func- tions of the ubiquitous albumin protein molecule. he albumin molecule has several characteristics that make it a unique protein. Most veterinarians are aware of the importance of this molecule in maintain- Ting colloid oncotic pressure, but albumin has many other less commonly recog- nized functions as well. The clinical consequences of hypoalbuminemia are reflections of the many functions albumin fulfills. Understanding the functions, synthesis, and *A companion article on degradation of the albumin molecule can improve understanding of the causes, conse- causes and treatment of quences, and treatment of hypoalbuminemia. hypoalbuminemia appears on page 940. STRUCTURE Email comments/questions to Albumin has a molecular weight of approximately 69,000 D, with minor variations [email protected], among species. -
Renal Sodium Handling in Minimal Change Nephrotic Syndrome
Arch Dis Child: first published as 10.1136/adc.59.9.825 on 1 September 1984. Downloaded from Archives of Disease in Childhood, 1984, 59, 825-830 Renal sodium handling in minimal change nephrotic syndrome A-B BOHLIN AND U BERG Department of Paediatrics, Karolinska Institute, Huddinge Hospital, Stockholm, Sweden SUMMARY Renal sodium handling was studied in 23 children at three different stages of the minimal change nephrotic syndrome-the oedema forming state, proteinuric steady state, and remission. Clearances of inulin and para-aminohippuric acid and urinary sodium excretion were determined basally, after intravenous infusion of isotonic saline and hyperoncotic albumin, and after furosemide injection. Absolute and fractional basal sodium excretion were significantly lower in oedema forming patients than in proteinuric patients in steady state, and non-proteinuric patients. In contrast to proteinuric patients in steady state and non-proteinuric patients, the oedema forming patients failed to respond to isotonic saline infusion with increased sodium excretion. After diuretic blockade with furosemide, the fractional sodium excretion of the oedema forming patients increased to values no different from those of the non-proteinuric patients, whereas the fractional sodium excretion of the steady state patients increased to significantly higher values. The plasma aldosterone concentration was within normal limits in 11 of 14 proteinuric patients, and did not correlate with the basal sodium excretion. Thus, sodium copyright. retention in the minimal change nephrotic syndrome was found only in oedema forming patients, and since this is not related to the plasma aldosterone concentration it may be caused by an intrarenal mechanism, probably sited in distal parts of the nephron. -
Kidney Questions
Kidney Questions Maximum Mark Question Mark Awarded 1 12 2 11 3 14 4 12 5 15 6 15 7 16 8 16 9 14 10 14 11 18 Total Mark Page 1 of 44 | WJEC/CBAC 2017 pdfcrowd.com 1. Page 2 of 44 | WJEC/CBAC 2017 pdfcrowd.com Page 3 of 44 | WJEC/CBAC 2017 pdfcrowd.com 2. Roughly 60% of the mass of the body is water and despite wide variation in the quantity of water taken in each day, body water content remains incredibly stable. One hormone responsible for this homeostatic control is antidiuretic hormone (ADH). (a) Describe the mechanisms that are triggered in the mammalian body when water intake is reduced. [6] (b) The graph below shows how the plasma concentration of antidiuretic hormone changes as plasma solute concentration rises. (i) Describe the relationship shown in the graph opposite. Page 4 of 44 | WJEC/CBAC 2017 pdfcrowd.com [2] (ii) Suggest why a person only begins to feel thirsty at a plasma solute concentration of 293 AU. [2] Secretion of antidiuretic hormone is stimulated by decreases in blood pressure and volume. These are conditions sensed by stretch receptors in the heart and large arteries. Severe diarrhoea is one condition which stimulates ADH secretion. (c) Suggest another condition which might stimulate ADH secretion. [1] Page 5 of 44 | WJEC/CBAC 2017 pdfcrowd.com 3. The diagram below shows a single nephron, with its blood supply, from a kidney. (a) (i) Name A, B and C shown on the diagram above. [3] A . B . C . (ii) Use two arrows, clearly labelled, on the nephron above, to show where the following processes take place: [2] I ultrafiltration; Page 6 of 44 | WJEC/CBAC 2017 pdfcrowd.com II selective reabsorption. -
L5 6 -Renal Reabsorbation and Secretation [PDF]
Define tubular reabsorption, Identify and describe tubular secretion, Describe tubular secretion mechanism involved in transcellular and paracellular with PAH transport and K+ Glucose reabsorption transport. Identify and describe Identify and describe the Study glucose titration curve mechanisms of tubular characteristic of loop of in terms of renal threshold, transport & Henle, distal convoluted tubular transport maximum, Describe tubular reabsorption tubule and collecting ducts splay, excretion and filtration of sodium and water for reabsorption and secretion Identify the tubular site and Identify the site and describe Revise tubule-glomerular describe how Amino Acids, the influence of aldosterone feedback and describe its HCO -, P0 - and Urea are on reabsorption of Na+ in the physiological importance 3 4 reabsorbed late distal tubules. Mind Map As the glomerular filtrate enters the renal tubules, it flows sequentially through the successive parts of the tubule: The proximal tubule → the loop of Henle(1) → the distal tubule(2) → the collecting tubule → finally ,the collecting duct, before it is excreted as urine. A long this course, some substances are selectively reabsorbed from the tubules back into the blood, whereas others are secreted from the blood into the tubular lumen. The urine represent the sum of three basic renal processes: glomerular filtration, tubular reabsorption, and tubular secretion: Urinary excretion = Glomerular Filtration – Tubular reabsorption + Tubular secretion Mechanisms of cellular transport in the nephron are: Active transport Pinocytosis\ Passive Transport Osmosis “Active transport can move a solute exocytosis against an electrochemical gradient and requires energy derived from metabolism” Water is always reabsorbed by a Simple diffusion passive (nonactive) (Additional reading) Primary active (without carrier physical mechanism Secondary active The proximal tubule, reabsorb protein) called osmosis , transport large molecules such as transport Cl, HCO3-, urea , which means water proteins by pinocytosis. -
Ludwig's Theory of Tubular Reabsorption: the Role of Physical Factors in Tubular Reabsorption
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 9 (1976) p. 313—322 EDITORIAL REVIEW Ludwig's theory of tubular reabsorption: The role of physical factors in tubular reabsorption From the very origins of physiology as a science, chet [2] created a sensation among physiologists and interest was focused on flow of body fluids. Beginning physicians alike. Quoting from a review [3], appear- with movement of fluid inside blood vessels and later ing in 1828 in the first volume of the American Jour- extending to that across membranes, physiologists nal of Medical Science, of Dutrochet's experiments: have sought mechanical explanations for these phe- "M. Dutrochet has recently published a work on vital nomena. The action of physicochemical forces across motion, in which he details experiments and discov- endothelial membrane structures is reasonably well eries, of a most interesting and extraordinary char- understood, at least in a qualitative sense; it is essen- acter, calculated to throw a new light upon an tially the same as for certain collodion membranes. important portion of physiology. ... M.Dutrochet On the other hand, there is as yet no general con- was, as yet, unable to assign a cause for this physico- sensus regarding the means by which physicochemical organic phenomenon, to which he applied the name forces influence convective flux (volume flux) across of endosmose." It appears to have been Graham who epithelial membranes. In fact, -
ANSWER KEY Integrative Sciences: Biological Systems B Body Fluid/Electrolytes and Kidney Systems
ANSWER KEY Integrative Sciences: Biological Systems B Body Fluid/Electrolytes and Kidney Systems Problem Set Review Monday, November 28, 2011 at 9 am Lecturer: Lisa M Harrison-Bernard, PhD I. Body Fluid Problems - Shifts of water between compartments What happens to the following 5 parameters: ECF volume? ICF volume? ECF osmolarity? Plasma protein concentration (PPC)? Blood pressure? A. Infusion of isotonic NaCl (isosmotic volume expansion) B. Diarrhea - loss of isotonic fluid (isosmotic volume contraction) C. Excessive NaCl intake - addition of NaCl (hyperosmotic volume expansion) D. Sweating in a desert - loss of water (hyperosmotic volume contraction) E. Syndrome of inappropriate antidiuretic hormone (SIADH) - gain of water (hypoosmotic volume expansion) F. Adrenocortical insufficiency - loss of NaCl (hypoosmotic volume contraction) Page 1 of 5 ECF ICF ECF PPC (g%) Blood Volume (L) Volume (L) Osmolarity Pressure (mOsm) (mmHg) A ⇑ ⇔ ⇔ ⇓ ⇑ B ⇓ ⇔ ⇔ ⇑ ⇓ C ⇑ ⇓ ⇑ ⇓ ⇑ D ⇓ ⇓ ⇑ ⇑ ⇓ E ⇑ ⇑ ⇓ ⇓ ⇑ F ⇓ ⇑ ⇓ ⇑ ⇓ Page 2 of 5 II. Starling Forces 1. At the afferent arteriolar end of a glomerular capillary, PGC is 45 mmHg, PBS is 10 mmHg, and πGC is 27 mmHg. What are the value and direction of the net ultrafiltration pressure? PUF = (PGC – PBS) – (πGC - πBS) PUF = (45 - 10 mmHg) – (27) = 8 mmHg favors filtration of fluid out of the glomerular capillary III. Renal Clearance, Renal Blood Flow, Glomerular Filtration Rate 2. To measure GFR: Infuse inulin intravenously until PIN is stable. Measure urine volume produced in a known period of time (urine flow). Measure PIN and UIN. Given the following: PIN = 0.5 mg/ml UIN = 60 mg/ml Urine flow = 1.0 ml/min Calculate GFR? GFR = CIN = (UIN)(UV) ÷ PIN GFR = (60 mg/ml) (1 ml/min) ÷ (0.5 mg/ml) = 120 ml/min 3. -
Excretory Products and Their Elimination
290 BIOLOGY CHAPTER 19 EXCRETORY PRODUCTS AND THEIR ELIMINATION 19.1 Human Animals accumulate ammonia, urea, uric acid, carbon dioxide, water Excretory and ions like Na+, K+, Cl–, phosphate, sulphate, etc., either by metabolic System activities or by other means like excess ingestion. These substances have to be removed totally or partially. In this chapter, you will learn the 19.2 Urine Formation mechanisms of elimination of these substances with special emphasis on 19.3 Function of the common nitrogenous wastes. Ammonia, urea and uric acid are the major Tubules forms of nitrogenous wastes excreted by the animals. Ammonia is the most toxic form and requires large amount of water for its elimination, 19.4 Mechanism of whereas uric acid, being the least toxic, can be removed with a minimum Concentration of loss of water. the Filtrate The process of excreting ammonia is Ammonotelism. Many bony fishes, 19.5 Regulation of aquatic amphibians and aquatic insects are ammonotelic in nature. Kidney Function Ammonia, as it is readily soluble, is generally excreted by diffusion across 19.6 Micturition body surfaces or through gill surfaces (in fish) as ammonium ions. Kidneys do not play any significant role in its removal. Terrestrial adaptation 19.7 Role of other necessitated the production of lesser toxic nitrogenous wastes like urea Organs in and uric acid for conservation of water. Mammals, many terrestrial Excretion amphibians and marine fishes mainly excrete urea and are called ureotelic 19.8 Disorders of the animals. Ammonia produced by metabolism is converted into urea in the Excretory liver of these animals and released into the blood which is filtered and System excreted out by the kidneys. -
Determinants of Glomerular Filtration in Experimental Glomerulonephritis in the Rat
Determinants of glomerular filtration in experimental glomerulonephritis in the rat. D A Maddox, … , T M Daugharty, B M Brenner J Clin Invest. 1975;55(2):305-318. https://doi.org/10.1172/JCI107934. Research Article Pressures and flows were measured in surface glomerular capillaries, efferent arterioles, and proximal tubules of 22 Wistar rats in the early autologous phase of nephrotoxic serum nephritis (NSN). Linear deposits of rabbit and rat IgG and C3 component of complement were demonstrated in glomerular capillary walls by immunofluorescence microscopy. Light microscopy revealed diffuse proliferative glomerulonephritis, and proteinuria was present. Although whole kidney and single nephron glomerular filtration rate (GFR) in NSN (0.8 plus or minus 0.04 SE2 ml/min and 2 plus or minus 2 nl/min, respectively) remained unchanged from values in 16 weight-matched NORMAL HYDROPENIC control rats (0.8 plus or minus 0.08 and 28 plus or minus 2), important alterations in glomerular dynamics were noted. Mean transcapillary hydraulic pressure difference (deltaP) averaged 41 plus or minus 1 mm Hg in NSN versus 32 plus or minus 1 in controls (P LESS THAN 0.005). Oncotic pressures at the afferent (piA) end of the glomerular capillary were similar in both groups ( 16 mm /g) but increased much less by the efferent end (piE) in NSN (to 29 plus or minus 1 mm Hg) than in controls (33 plus or minus 1, P less than 0.025). Hence, equality between deltaP and piE, denoting filtration pressure equilibrium, obtained in control but not in NSN rats. While glomerular plasma flow rate was slightly higher […] Find the latest version: https://jci.me/107934/pdf Determinants of Glomerular Filtration in Experimental Glomerulonephritis in the Rat D. -
Renal Function in Primary Aldosteronism
RENAL FUNCTION IN PRIMARY ALDOSTERONISM Harriet P. Dustan, … , A. C. Corcoran, Irvine H. Page J Clin Invest. 1956;35(12):1357-1363. https://doi.org/10.1172/JCI103392. Research Article Find the latest version: https://jci.me/103392/pdf RENAL FUNCTION IN PRIMARY ALDOSTERONISM 1 By HARRIET P. DUSTAN, A. C. CORCORAN, AND IRVINE H. PAGE (From the Research Division of The Cleveland Clinic Foundation and The Frank E. Bunts Educational Institute, Cleveland, 0.) (Submitted for publication June 11, 1956; accepted August 9, 1956) Primary aldosteronism is characterized by weak- purate (PAH) and mannitol. Total renal vascular re- ness-a sequel to potassium loss; hypertension- sistance was calculated by the formula of Gomez (3). The functions of water conservation and electrolyte ex- attributed to sodium retention; thirst and polyuria; cretion were observed simultaneously. Water con- and excretion of dilute, alkaline urine (1). These servation was determined from the differences (TVio) defects imply significant changes in renal function. between urine flow (V) and osmolal clearance (Co..) The purpose of this report is to describe pre- (4) during osmotic diuresis in hydropenia (water depri- and postoperative observations of renal function vation for 16 or 24 hours and/or infusion of Pitressin@). The priming solution contained 260 mOsm. of mannitol in three patients suffering from aldosterone-se- and 0.6 gin. of PAH; the sustaining infusion supplied creting adrenal cortical tumors. about 3 mOsm. of mannitol and 15 mg. per PAH per min- The data indicate that excess urinary potassium ute. Urine formed during the first 20 minutes was dis- excretion is attributable to aldosteronism as such, carded; it was then collected from an indwelling urethral and may bear on the basic cellular mechanism of catheter at 3 to 6 successive intervals of about 10 min- action of aldosterone. -
Glomerulonephritis Management in General Practice
Renal disease • THEME Glomerulonephritis Management in general practice Nicole M Isbel MBBS, FRACP, is Consultant Nephrologist, Princess Alexandra lomerular disease remains an important cause Hospital, Brisbane, BACKGROUND Glomerulonephritis (GN) is an G and Senior Lecturer in important cause of both acute and chronic kidney of renal impairment (and is the commonest cause Medicine, University disease, however the diagnosis can be difficult of end stage kidney disease [ESKD] in Australia).1 of Queensland. nikky_ due to the variability of presenting features. Early diagnosis is essential as intervention can make [email protected] a significant impact on improving patient outcomes. OBJECTIVE This article aims to develop However, presentation can be variable – from indolent a structured approach to the investigation of patients with markers of kidney disease, and and asymptomatic to explosive with rapid loss of kidney promote the recognition of patients who need function. Pathology may be localised to the kidney or further assessment. Consideration is given to the part of a systemic illness. Therefore diagnosis involves importance of general measures required in the a systematic approach using a combination of clinical care of patients with GN. features, directed laboratory and radiological testing, DISCUSSION Glomerulonephritis is not an and in many (but not all) cases, a kidney biopsy to everyday presentation, however recognition establish the histological diagnosis. Management of and appropriate management is important to glomerulonephritis (GN) involves specific therapies prevent loss of kidney function. Disease specific directed at the underlying, often immunological cause treatment of GN may require specialist care, of the disease and more general strategies aimed at however much of the management involves delaying progression of kidney impairment. -
Renal Hemodynamic and Metabolic Physiology in Normal Pregnancy
Obstetric Nephrology: Renal Hemodynamic and Metabolic Physiology in Normal Pregnancy Ayodele Odutayo and Michelle Hladunewich Summary Glomerular hyperfiltration, altered tubular function, and shifts in electrolyte-fluid balance are among the hallmark renal physiologic changes that characterize a healthy pregnancy. These adjustments are not only critical to maternal and fetal well being, but also provide the clinical context for identifying gestational aberrations in Divisions of Nephrology and renal function and electrolyte composition. Systemic vasodilation characterizes early gestation and produces Obstetric Medicine, increments in renal plasma flow and GFR, the latter of which is maintained into the postpartum period. In addition, Department of renal tubular changes allow for the accumulation of nutrients and electrolytes necessary for fetal growth such that Medicine, wasting of proteins, glucose, and amino acids in urine is limited in pregnancy and total body stores of electrolytes Sunnybrook Health increase throughout gestation. Substantial insight into the mechanisms underlying these complex adjustments can Sciences Centre, University of Toronto, be gleaned from the available animal and human literature, but our understanding in many areas remains Toronto, Ontario, incomplete. This article reviews the available literature on renal adaptation to normal pregnancy, including renal Canada function, tubular function, and electrolyte-fluid balance, along with the clinical ramifications of these adjust- ments, the limitations of the existing literature, and suggestions for future studies. Correspondence: Clin J Am Soc Nephrol 7: 2073–2080, 2012. doi: 10.2215/CJN.00470112 Dr. Michelle Hladunewich, Divisions of Nephrology, Critical Introduction clinically presents as a decrease in the serum creati- Care, and Obstetric Maternal accommodation to normal pregnancy begins nine.