Renal Physiology – Glomerular Filtration, Tubular Reabsorption & Secretion

Renal physiology is the study of the physiology of the kidney, specifically at the level of the nephron, which is the smallest functional unit of the kidney where blood entering the kidney goes through the process of filtration.

Overview of Renal Physiology

3 Important Functions of the Nephrons:

  • control blood concentration and volume through selected removal of water and solutes
  • regulate blood pH
  • remove toxic waste from the blood

Through these functions, materials from the blood is removed, others which are required are returned, and the remaining unneeded material is excreted collectively as urine. In other words, urine formation requires Glomerular Filtration, Tubular Reabsorption and Tubular Secretion.

Renal Physiology – Glomerular Filtration

Glomerular Filtration occurs in the renal corpuscle of the kidneys across the endohelial-capsular membrane, which results in the fluid called glomerular filtrate ( 150 lt in adult females; 180 lt in adult males). The blood plasma in the afferent arterioles which become the glomerular filtrate is called the filtration fraction.

renal physiology
Retrieved from https://slidetodoc.com/renal-functions-gfr-learning-objectives-enumerate-general-functions/ on 5th December 2021
renal physiology
Retrieved from https://slideplayer.com/slide/10629513/36/images/34/Glomerular+Filtration.jpg on 15th December 2021

Understanding the Glomerular Filtration Process

Pressures Causing Filtration & GFR Regulation

The Glomerular Filtration Rate (GFR) is the amount of filtrate formed in all the renal corpuscles of both kidneys per minute (rate in males = 125ml/min; rate in females = 105ml/min). Maintenance of a constant GFR ensures that useful substances are not lost.

A change in GFR indicates a change in the net filtration pressure – if the glomerular blood hydrostatic pressure (GBHP) falls to 45mmHg, the filtration process is halted as the opposing pressures equal to 45mmHg.

There are 3 mechanisms which control GFR by adjusting the blood flow into and out of the glomerulus, and by altering the glomerular capillary surface area for the process of filtration:

  1. Renal Autoregulation: Through the Myogenic Mechanism, stretching triggers contraction of smooth muscle cells in the afferent arteriole wall, causing normalisation of the renal blood flow and GFR within seconds following a change in blood pressure. Additionally, through the Tubuloglomerular Feedback, increased distal tubular sodium chloride concentration causes the release of adenosine, leading to a series of events that help regulate the GFR.
  2. Neural Regulation: The Sympathetic Nervous System, which supplies the renal blood vessels, is responsible for the release of norepinephrine. Through Moderate Sympathetic Stimulation, norepinephrine activates the a1 (alpha-1 adrenergic) receptor in the afferent and efferent arterioles, causing vasoconstriction, causing blood flow restriction, leading to a slight GFR decrease. In Greater Sympathetic Stimulation, vasoconstriction of the afferent arterioles predominates; blood flow in the glomerular capillaries is decreased, leading to a decrease in GFR.
  3. Hormonal Regulation: Angiotensin II, which is a vasoconstrictor, acts on the afferent and the efferent arterioles, reducing blood flow leading to a decrease in the GFR. Additionally, Atrial Natriuretic Peptide (ANP) is released through the stretching of the atrial walls when there is an increase in blood volume, leading to an increase in capillary surface area, causing an increase in the GFR.

Renal Physiology – Tubular Reabsorption

In the average adult, the Glomerular Filtration Rate (GFR) is approximately 125ml/min, meaning that around 180 litres are filtered in one day. However, only around 1ltr a day is excreted as urine by the body. This happens because throughout the filtration process, around 99% of the filtrate is reabsorbed back into the blood in what is called tubular reabsorption.

In tubular reabsorption, the proximal convoluted tubule cells process and reabsorb over 80% of the glomerular filtrate, whilst other parts of the nephron ensure homeostasis by controlling excretion amounts of electrolytes, water and hydrogen ions. Through tubular reabsorption, the following are reabsorbed back into the blood stream:

  • Sodium
  • Potassium
  • Calcium
  • Chloride
  • Bicarbonate
  • Phosphate

Peptides and small proteins are also reabsorbed through pinocytosis.

Substances completely reabsorbed from the filtrate are:

  • Water
  • Proteins
  • Chloride
  • Sodium
  • Bicarbonate
  • Glucose
  • Potassium

Urea and Uric Acid are partially reabsorbed from the filtrate.

renal physiology
Retrieved from https://baujiti.home.blog/2013/09/25/urine-formation-form-iii/ on 5th December 2021

Renal Physiology – Tubular Secretion

Tubular Secretion, which occurs in the proximal and distal tubules as well as in the collecting dugt, removes certain materials from the body such as Potassium ions, Hydrogen ions, Ammonium ions, Creatinine, and drugs.; it also helps control the blood’s pH.

Renin-Angiotensin-aldosterone System (RAAS)

RAAS
Retrieved from https://step1.medbullets.com/renal/115016/renin-angiotensin-aldosterone-system on 15th December 2021

Aldosterone causes increased sodium and water reabsorption from the distal tubule and collecting ducts, leading to an increase in the extracellular fluid volume. This allows the restoration of the blood pressure to its normal state. Additionally, Aldosterone has an affect on the secretion of potassium by the distal convoluted tubule and collecting duct.

Antidiuretic Hormone

The AntiDiuretic Hormone, which is produced by the hypothalamus, controls the concentration of the urine to be excreted.

When the blood-water concentration is low, ADH is released, which increases the permeability of the plasma membranes of the cells of the distal tubules and the collecting ducts. Increased permeability causes more water molecules to pass into the cells, and then into the blood.

With no ADH, the ducts become impermeable to water, causing water to be expelled into urine.

Atrial Natriuretic Peptide

Increased blood volume causes the atrial walls to stretch, leading to the release of the Atrial Natriuretic Peptide (ANP). ANP inhibits the reabsorption of sodium and water in the proximal convoluted tubule and collecting duct, suppresses the secretion of aldosterone, and suppresses the secretion of ADH. This results in increased excretion of sodium ions (natriuresis) and increased urine output (diuresis), leading to a decrease in the blood volume and blood pressure.

Note…

Tubular Reabsorption REMOVES substances from the filtrate into the blood… Tubular Secretion ADDS materials to the filtrate from the blood.

Renal Physiology – Solute Reabsorption

Solute Reabsorption happens within the ascending limb of the loop of henle.

Summary…

Retrieved from https://www.researchgate.net/figure/Nephron-segments-and-their-main-physiological-function-The-nephron-is-the-functional_fig1_321907177 on 15th December 2021

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RAAS Renin-Angiotensin Aldosterone System: CV Drugs Affecting RAAS

This post features a collection of videos that provide a visual approach on cardiovascular pharmacology for student nurses, specifically on anti-hypertensives affecting RAAS.

Cardiovascular pharmacology deals with the study of the effects of drugs upon the heart or circulatory system. Cardiovascular medicines help to prevent and treat cardiovascular disease, slow the progression of it as well as treat its symptoms whilst providing a better quality of life and increasing life expectancy.

Types of Cardiovascular Drugs include:

  • Anti-Hypertensive Drugs
  • Anti-Angina Drugs
  • Anti-Arrhythmic Drugs
  • Anti-Coagulants
  • Anti-Hyperlipidaemic Drugs

Anti-Hypertensive Drugs are further sub-divided into 4 categories, namely:

Renin-Angiotensin Aldosterone Inhibitors

Adregenic System Inhibitors

Diuretics

Direct Vasodilators

Below you can find a collection of videos that can help provide a more visual approach to cardiovascular pharmacology, specifically on the Anti-Hypertensive DrugsRenin-Angiotensin Aldosterone Inhibitors RAAS.


RAAS – Renin-Angiotensin Aldosterone System

The RAAS system regulates the blood volume and the systemic vascular resistance, affecting the cardiac output (bloodflow) and arterial pressure, and impacting Renin, Angiotensin and Aldosterone.

ACE Inhibitors:

ACE inhibitors end with _pril eg. Enalapril, Lisinopril, Perindopril.

  • Block the conversion of Angiotensin 1 to Angiotensin 2 = decrease in BP, peripheral volume, heart workload, blood volume, aldosterone secretion.
  • INDICATIONS: hypertension, heart failure, left ventricular hypertrophy.
  • SIDE EFFECTS: headache, dizziness, tiredness, hypotension (especially after 1st dose; ideally administer before going to bed at night), reflex tachycardia, arrhythmias, decreased renal function, dry persistent non-productive cough, angioedema (breathing problems), rash, taste disturbances, hyperkalaemia.
  • NURSING INTERVENTION: avoid abrupt stopping of medication, take 1hr before or 2hrs after a meal, monitor patients with risk of dehydration, check blood profile for electrolytes and creatinine, monitor BP, avoid NSAIDs to minimise renal damage risk, stop additional K+ sparing diuretics and K+ supplements as they would increase the risk for hyperkalaemia.

ARBs – Angiotensin II Receptor Blockers:

ARBs end with _sartans eg. Candesartan, Losartan, Eprosartan.

  • Block Angiotensin II from binding with receptors in the smooth muscles of the heart and blood vessels = reduction in vasoconstriction, aldosterone secretion, catecholamine release, cell growth and BP.
  • No effect on bradykinin thus no non-productive cough is experienced as a side effect.
  • INDICATIONS: hypertension, HF, LVF (left ventricular failure), patients unable to take ACE inhibitors eg. those experiencing dry cough.
  • ADVERSE EFFECTS: headache, dizziness, weakness, orthostatic hypotension, URTI (upper respiratory tract infections), mild cough, diarrhoea, abdominal pain, nausea, dry mouth, tooth pain, rash, alopecia, dry skin.

Renin Angiotensin Aldosterone System (RAAS)

ACE Inhibitors

Angiotensin II Receptor Blockers ARBs

Special thanks to the creator of the featured videos on this post, specifically Youtube Channel Registered Nurse RN.

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