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GFR or tubular function

test will allow us to see which kidney problems there are ans how far the problems are.

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receptors: osmoreceptors (in hypothalamus) & baroreceptors, which stimulate

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hypertonicity: many solutes not enough water
hypervoleamia: too much water
hypertension: high BP

Not only kidneys are related to these processes, also:
- Heart, with baroreceptors
- Hypothalamus in brain, with osmoreceptors

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easiest test, it looks at:
- look at color (blood?)
- volume, nocturia
- specific gravity (weight of particles) or osmolality (number of particles)
- pH (normal = 5.5-6.5)

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dipstick uses reactants fixed on pods that change color on reacting with specific elements in urine. Elements such as: blood, protein, glucose, bacteria/WBCs

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urea, blood urine nitrogen,  phosphorus level, creatinine, electrolytes (chlorides), cells (RBCs, WBCs). Vit. D deficiency

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produced in hypothalamus and stored in pituitary gland.

effect: principal cells in cortical colecting duct, which allows for moe aquaproins

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a-intercalated cells

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100% of glucose, amino acids is reabsorbed & Na, K, bicarbonate, water, urea

biggest % is recovered in the first part of the nephron and becomes less in more distal parts

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b-intercalacted cells

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asses the kidney itself or the pipes

the size of the kidney is important. The condition of the kidney (fibrotic?). How do we see the cortex, medulla? Identify this using images.

kidney stones: x-ray, US or CT
pyelography: inject contrast and you can see where a blockage is present in the ureter for example

biopsy:
when you're suspect a malignancy or when you see in the lab elements of a nephritic or nephrotic elements and you want to see where the problem is.
- Kidney biopsy is more frequent than in other organs.

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urine cannot be lower than pH=4, so buffers are needed to excrete more H+'s

2 types:
1. Ammonia buffer: NH3 goes into proximal tubule  + H to form NH4 which can be excreted in urine

2. monohydrogen phosphate is able to bind H+ = H2Po4, which can be excreted

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2 components: ascending & descending

1. descending limb: reabsorption of water via osmosis with aquaporins. impermeable to solutes (hypertonic)
2. ascending limb: permeability to sodium and impermeable to water and urea  (low osmotic pressure and sodium can diffuse into interstitium, because water was absorbed before in the descending limb = countercurrent multiplier mechanism -->  The water follows the sodium) (hypotonic)

Vasa recta: part of countercurrent multiplier mechanism. facilitates movement of the substances.  Branch of peritubular capillaries in medulla that help balance water and NA in the interstitium. Rapid removal of salts, to prevent the salts to be washed away

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Excretion of urea:
Urea recycling --> helps pull ou the water, because urea makes it more salty/osmotic

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On the apical membrane, NaCl importers and channels. Regulated by aldosterone in the distal part of the DCT.

Basolateral membrane: Primary active Na transport & Ca reabsorption (ATP-dependent)

Aldosterone is produced in response to hyperkalemia and AII.
-  acts on principal cells of the late DCT
- transporters inside the cell: lipid bilayer and activated transcription factors (3 different activator: epithelial sodium channels, pump Na out of cell and lastly, K outside the cell))

active PTH:
- Calcium is absorbed via passive potassium uptake
- low blood Ca, leads to PTH production/activation which activates Calcium channels in luminal membrane of the cell. This allows Ca to enter the cell from the filtrate more passively, because there is more Ca in the cell than in the blood, so a secondary active pump is used for Ca.

ADH
- intercalated a and b cells (associated with acid base regulation)
- recycle HCO3
- in a-cell, in acidosis, it gets rids of H via co-transporter and leads to increase of H inside the a-cells and thereby gets rid of ADH
- b-cells do the complete opposite

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important: different segments and their functions! (cellular components & channels)!

Overview:
- filters blood and regulates fluid-electrolyte balance
- acid base balance
-produces hormones

kidney (besides kidney, kidney is main) is only organ capable of gluconeogenesis. Kidney produces enough to release into circulation

renal corpuscle = glomerulus + bowman's capsule

Tubule= proxima + loop of henle + distal + collecting duct

Functional structure:
arteriors:
- afferent, arise from interlobular arteries and supply glumeral bed and drain into peritubular network
- efferent

Glomerular capillary wall:
- lamina rare interna / endothelium allows blood component  to go through (electrolytes, water, small proteins), but not RBC, WBC and platelets
- basement membrane: negatively charged, prevents proteins from passing through
- lamina rera externa (=podocytes): cells of the capsule that wrap around capillaries, its useful for selective filtration. visceral epithelium cells, support the basement membrane. foot processes allowing anchoring onto capillaries and they hang into bowman's space.

Filtration:
- GFR = glomerular filtration rate. volume of fluid filtered into bowman's capsule per unit of time.
- normal GFR: 170-180 L/day
- depends on sex and age

filtration coefficient. surface are + permeability.

3 forces influence GFR:
1. blood pressure
2.  oncotic pressure (plasma proteins)
3. capsular hydrostatic pressure (build up pressure pressing outwards in Bowman's capsule)
--> efferent will narrow so that it won't be easy to pass the blood (more time spent on the glomerulus)

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low blood pH, first you increase RR, but later on kidney will produce and secrete bicarbonate into the blood. For every bicarbonate produced by the kidney, ,1 H+ will be secreted by the kidney

To decrease pH: the opposite, kidney holds onto the H+

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passes close to the glomerulus. They are specialized cells in the wall of DCT and are sensitive to NaCl concentration. If NaCl is low, there will be decreased resistance to blood flow in resistance to bring GFR back to normal

macula densa will increase renin release from the JXA. JXA regulates flow and pressure in the tubules.

JXA is important! Know structure & function

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in acidosis.

Anion gap helps us in acidosis to see where the problem comes from. It is measure in blood. Which will support your clinical assessment. Useful tool is you have a doubt where the acid is coming from. It will add to the assessment of the patient.

anion gap used to identify if it is due to retention of the acid. you look at normal cations present in the plasma and then the normal anion present. the sums of the - and + charges should be equal. useful: measurements of ions are easily available

normal: 12-16 mmol/L

acidosis with normal or high anion gap. Normal: HCl is being retained and in high HCO3 is lost.

causes: increased HCl production, increased bicarbonate loss in GI (diarrhea)

Different types:
renal tubular acidosis:
- type 4: unresponsiveness to aldosterone
type 3: rare, combination of type 1+2
- type 2: proximal renal tubular acidosis
- type 1: distal tubular acidosis. failure of H+ secretion

High anion gap:
- anions present in increased quantities.
- e.g. CKD or lactic acidosis

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rise is plasma osmolality which is detected. posterior pituitary gland senses this and releases renin. Renin converts angiotensinogen into AI. AI is converted into AII by ACE. AII has 2 actions:
1. AT1-receptor: mediates vasoconstrictor
2. AT2-receptor: increased production of aldosterone, which causes kidneys to reabsorb Na (--> plasma osmolality goes down, also because more water goes into the fluid)

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atrial natriuretic peptide: secreted by atrial cells in heart when heart stretches, which results in sodium and water excretion is increased. GFR also increases. It is also a vasodilator

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creatinine clearance: it is filtered at glomerulus. Calculate to my urine concentration x flow rate x plasma concentration creatinine

it needs to be adjusted for weight, body composition. age, life style. Why? it is a waste product of muscles. So it difference between athletic person vs non-athletic person, because of the difference in muscle mass.

creatinine does not rise above normal range until there is a reduction of 50-60% in GFR

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Respiratory acidosis
= when ventilation is disturbed and body cannot get rid of Pco2. Increase in CO2 and bicarbonate
- common causes: COPD, pulmonary edema, asthma
- increase removal of CO2, fall in pco2 & rise H+
- what causes hyperventilation? anxiety attack, hypoxia (high altitudes)
--> mainly dependent of CO2

metabolic acidosis:
low pH & presence of acids.
- decrease of H+, loss of bicarbonate, ketoacidosis, lactoasicodis

metabolic alkalosis:
increased pH (alkali are added or acids are removed)
different classifications, dependent on underlying pathology:
- chloride depletion, most common
- K depletion
- combination of K and Cl depletion
--> very common, 50% of acid base disorders,