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31 Cards in this Set

  • Front
  • Back
Basic kidney functions
Water and electrolyte homeostasis

Acid – base balance

Elimination of waste products and ingested chemicals

Hormone production
Mechanisms of renal excretion
180 l glomerular filtrate per day (2 ml/s)

99% - back reabsoption

Renal perfusion at rest = 20% of cardiac output (this is higher than in heart, brain and liver
Glomerular filtration rate
Balance of hydrostatic and osmotic pressures acting across diffusion barrier (endotelium fenestrae, basement nenbrane, slit diaphragms betweens the podocytes)
Factors determining GFR:
Surface area (1 milion nephrons within each kidney)
Permeability
Net filtration pressure (NFP) across diffusion barrier
filtration koefficient (Kf)
surface are and permeabiltiy
Disturbances of glomerular function
Decrease of glomerular filtration
Increase of glomerular permeability
Decrease of glomerular filtration
Decr. renal blood flow
stenosis of renal artery

Decr. glomerular capillary hydrostatic pressure (PGC)
hypovolemia, circulatory shock

Incr. hydrostatic pressure in Bowman´s capsule (PT)
block of fluid flow ( intra- and extrarenal)

Decr. concentration of plasma proteins (GC)

Decr. Kf
Decr. effective filtration surface area
Increase of glomerular permeability
Glomerular proteinuria

Size-selective properties of the glomerulus
Charge-selective propeties of the glomerulus
Hamodynamic forces operating across the glomerulus
Selective proteinuria
Albumin
Small amount of low-molecular globulins
Non-selective proteinuria
Albumin
Globulins of various molecular weight
Tubular proteinuria
Decr. excretion of low molecular proteins

alpha 1-microglobulin, beta 2-microglobulin
Overload (prerenal) proteinuria
Small molecular weight proteins can rise when are synthetised in excess

Tissue degraded products
Proteins of acute phase (pyretic proteinuria)
Myoglobin (rhabdomyolysis)
Ligfht immunoglobulin chains (myeloma)
Proteinuria-Values
Healthy adult subject:
Small proteinuria:
Heavy proteinuria:
Healthy adult subject
No more than 150 mg/day

Small proteinuria
1 g/day

Haevy proteinuria
3,5 g/day and more
Nephrotic syndrome (10 – 30 g/day)
Renal hematuria
Glomerular
Abnormally increased permeability

Non-glomerular
Rupture of tumor or cyst vessels

Bleading from urinary tract
Relation between the reduction of GFR and excretion function of kidneys
 GF   retention of substrates

1. urea, creatinín
2. phosphates, K+, H+
3. NaCl
Reabsorption of glucose, amino acids, Na, K, Cl, H2O
Proximal tubule (Na, Glu -Countertransport) ; (Na, H+ -Countertransport)
Thick ascending limb of loop of Henle (Na, K, Cl,)
Distal tubule (Na,Cl)
Disturbances of tubular functions
Tubular proteinuria
Glucosuria
Aminoaciduria
Diabetes insipidus
Osmotic diuresis
Diabetes insipidus
Neurogenic (Decr.ADH)
Nephrogenic (insensitivity of the renal tubule to ADH)
Osmotic diuresis
Pressure of large quantities of unreabsorbed solutes in the renal tubules >>increase in urine volume
Unreabsorbed solutes in the proximal tubules „hold water in the next tubules“
Hydrogen ion secretion and bicarbonate reabsorption

Renal tubular acidosis
- impairment of the ability to make the urine acidic
- chronic renal disease – reduction of secreted hydrogen ion
because of impaired renal tubular production of NH4+
Disturbances of kidney ability to concentrate urine
Disturbances of water reabsorption
Disturbances of the production of medullar
Disturbances of water reabsorption
diabetes insipidus
Disturbances of the production of medullar hyperosmolarity
- osmotic diuresis
- incr. blood flow in vasa recta
- morphologic deformations of medulla
Proteinuria:
3.5 g or more of protein in the urine per day
Minimal changes of glomerular membrane: 90% albumin (selective proteinuria)
Hypoproteinemia (hypoalbuminemia)
Mechanisms: proteinuria +
Protein loss by stool
Plasma proteins are shifted to extravascular space
Increased albumin katabolism
Inadequately increase albumin synthesis in liver
Hyperlipidemia
Incresed lipoprotein synthesis in liver
Mechanisms of edema in nephrotic syndrome (NS)
Classis theory
Hypoalbuminemia   plasma oncotic pressure  hypovolemia  R-A-A + ADH  Na + water retention

!!! But hypovolemia is present only in 30% of patients suffering from NS; plasma renin activity and aldosteron are decreased
Two groups of patients with NS:
1. Hypovolemia and  R-A-A activity
- small glomerular abnormalities
2.Hypervolemia without R-A-A activation
- more serious morphological abnormalities
Pathophysiology of edema formation
Extracellular fluid volume is determined by the balance between Na intake and its renal excretion

Common feature: renal salt retention despite progressive expaansion of ECF volume

Primary abnormality of the kidney
Secondary response to some disturbances in the circulation
Primary edema (overfill)
Primary defect in renal sodium excretion

Hyperevolemia leads to high cardiac output

 R-A-A,  ADH,  sympathetic activity

Examples: blomerulonephritis, renal failure
Secondary edema (underfill)
Response of normal kidnay to actual or sensed underfilling of the circulation

Primary disturbances within the circulation secondary triggers renal sodium retention

inr. R-A-A, incr. ADH, incr. sympathetic activity

Effective arterial blood volume