Unit VIII

Disorders of Renal Function

and Fluids and Electrolytes

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Lecture One: Lecture Two:
 Anatomy and  Acid base balance
Physiology revision  Urinary obstructive
 Alterations in fluid disorders
and electrolytes  Stones
 Infections
 Renal failure
(acute/chronic)

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 Structure:
 Paired, bean-shaped organs
 Multilobular structure, composed of up to 18 lobes
 Each lobule is composed of nephrons, the functional
units of the kidney
 Location :
 Outside the peritoneal cavity in the back of the upper
abdomen
 One on each side of the vertebral column at the level of
the 12th thoracic to 3rd lumbar vertebrae

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 Medulla
Renal cortex
Renal pyramid

Renal column
Renal papilla

Renal pelvis

Calyx

Ureter
Renal capsule

Calyx, renal cortex, ureter, renal

Pathophysiology 2 - pelvis,
Naturopathyrenal
- Ryka capsule, renal column,
renal papilla, renal pyramid, medulla
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 Functional units of the kidney composed of
a glomerulus and a tubule. 1 million units
per kidney.
 85% are cortical, the others are
juxtamedullary.
 Reabsorb water, electrolytes, and other
substances needed to maintain the
constancy of the internal environment into
the bloodstream.
 Secrete other unneeded materials into the
tubular filtrate for elimination.
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 1. Glomerular capsule
2. Glomerulus
3. Afferent arteriole
4. Efferent arteriole
5. Proximal convoluted
tubule
6. Distal convoluted tubule
7. Collecting duct
8. Loop of Henle
9. Peritubular capillary

Afferent arteriole, Collecting duct, Distal convoluted tubule, Efferent

arteriole, Glomerular capsule, Glomerulus,
Pathophysiology Loop
2 - Naturopathy - Ryka of Henle, Peritubular
capillary, Proximal convoluted tubule Moore 2010 6
 Uric acid is a product of purine metabolism
 High levels in blood can cause gout
 High levels in kidneys can cause stones
 Absorption usually exceeds secretion, but
people with excess uric acid secrete less than
people with normal levels.
 Uric acid use same transport mechanism for
secretion as aspirin, thus aspirin is not
recommended for people with gout.
 Diuretics may increase the re-absorption of uric acid

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 Urea is a by-product of protein metabolism
 Levels increase with high protein diets,
excessive tissue breakdown, or in presence of
GI bleeding.
 The kidneys regulate urea levels (known as
BUN - blood urea nitrogen).
 A high GFR decreases reabsorption of urea.
 A slow GFR increases reabsorption of urea in
tubules.

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 Regulation of blood pressure:
 Via the renin-Angiotensin-Aldosterone Mechanism
 Synthesis of Erythropoietin:
 Regulates the differentiation of red blood cells in
bone marrow
 Activation of Vitamin D:
 Increases calcium absorption from the
gastrointestinal tract
 Helps regulate calcium deposition in bone

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 Most act by decreasing re-absorption of sodium and
water by kidneys.
1) Loop diuretics:
 Exert their effect in the thick ascending loop of Henle
2) Thiazide diuretics:
 Prevent the reabsorption of NaCl in the distal convoluted
tubule
3) The aldosterone antagonists (potassium-sparing
diuretics):
 Reduce sodium re-absorption and decrease potassium
secretion in the late distal tubule and cortical collecting
tubule site regulated by aldosterone (please note the
error in your book page 736 and replace “increase” with
“decrease” in the “aldosterone antagonists” chapter.)
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 Progressive decline in kidney function.
 By age 70, rate of filtrate formation is only about
half that of the middle-age adult. May results
from impaired renal circulation due to
atherosclerosis which affects the entire
circulatory system of an aging person.
 Decrease in the number of functional nephrons,
plus tubule cells become less efficient in ability
to concentrate urine.

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 Bladder shrinkage and loss of bladder tone 
many experience:
 Urgency
 Frequency
 Nocturia
 Incontinence
 Urinary retention (most often as result of
hypertrophy of prostate gland in males)

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 Urinalysis
 Glomerular filtration rate
 Blood tests
 Serum creatinine
 Blood urea nitrogen (BUN)
 Cystoscopy
 Ultrasonography
 Radiological and other image studies

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  A palpable swelling produced by expansion of
interstitial fluid volume.
 Not obvious until interstitial volume has
increased by 2.5 to 3.0 L
 Causes - Chart 31.1 (p. 768)
 Increased capillary pressure
 Decreased colloidal osmotic pressure
 Increased Capillary permeability
 Obstruction of lymphatic flow a.k.a.
lymphoedema (infection)

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  Elephantiasis occurs
in the presence of
microscopic, thread-
like parasitic worms
such as Wuchereria
bancrofti, Brugia
malayi, and B. timori,
all of which are
transmitted by
mosquitoes.

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 Oedema
Formerly known as “dropsy” or “hydropsy”.
 Types:

 Pitting
oedema
 Non-pitting oedema
 Brawny oedema
 Treatment:
 Elevation of feet
 Diuretics
 Elastic support stockings and sleeves

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 increased hydrostatic pressure;
 reduced oncotic (protein) pressure within
blood vessels;
 increased tissue oncotic pressure;
 increased blood vessel wall permeability e.g.
inflammation;
 obstruction of fluid clearance via the lymphatic
system; (plus radiotherapy etc)

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  Diabetes insipidus resembles
diabetes mellitus because the
symptoms of both diseases are
increased urination and thirst. 
 However, in every other
respect, including the causes
and treatment of the disorders,
the diseases are completely
unrelated.  
 Sometimes diabetes insipidus is
referred to as "water" diabetes to
distinguish it from the more
common diabetes mellitus or
"sugar" diabetes.

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 Diabetes insipidus (p774)

A deficiency of or a decreased response to ADH

 Two types:
 Neurogenic: defect in synthesis or release of ADH
 Loss of neurons (75-80% needed for evidence of
polyuria).
 Nephrogenic: kidneys not responding
(insenesitive) to ADH.
 Causes: Genetic/lithium use/hypercalcaemia/
potassium depletion
 Symptoms:
 Urine excretion between 3 - 20 L/day
 Excessive thirst
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 Electrolytes imbalances
Regulation (n=5)
 Sodium and water (p.775)
 Potassium (p.783)

Commences p790
 Calcium (p.792)

 Phosphate (p.797)

 Magnesium (p. 800)

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 1. Electrolytes imbalances
Sodium
Hyponatraemia (p779)
 Causes:
 drugs (diuretics and drugs increasing ADH levels)
 inappropriate fluid replacement during heat exposure
or heavy exercise
 polydipsia in psychotic disorders
 Signs & Symptoms:
 ICF oedema, muscle cramps, weakness, fatigue.
 GI disorders: vomiting, diarrhoea, abdominal cramps,
and nausea.
 If severe, brain and NS will be affected: apathy,
lethargy, and headache to seizures and coma
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 Electrolytes imbalances
Sodium

 Hypernatraemia (p780)
Most likely to occur in infants and people who
cannot ask for water.
 Causes: mostly from loss of body fluids e.g.
from increased losses of respiratory tract
during fever or strenuous exercise, from
diarrhoea (infection etc).
 Signs & Symptoms: thirst. If severe: body
weight loss increased, BP drops, skin and
mucous membranes dry up.
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 2. Electrolytes imbalances
Potassium
Hypokalaemia (p785)
 Causes:
 Excessive losses (diuretic therapy/
sweating/ diarrhea)
 Inadequate intake (diets/elderly)
 Increased movement of K into cells

 Signs& Symptoms: Renal, gastrointestinal,

cardiovascular, and skeletal muscle
function (Table 33.8).
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Hypokalaemia has a paradoxical effect on the
muscular and cardiovascular systems. It makes
skeletal muscles (esp. legs) weak while the
cardiac system is hyperactive (arrythmias.).

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  A 35-year-old man, who had been
ingesting one or two bags of tablets
of pure licorice daily (20–40 g/day)
for about two years, developed an
acute myopathy with high levels of
serum muscle enzymes and the
typical features of mineralocorticoid
excess: serious hypokalemia,
hypertension, metabolic alkalosis.
 A component (glycyrrhizin) ,in
licorice has an aldosterone like
activity which causes the
excretion of potassium.

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 Electrolytes imbalances
Potassium
Hyperkalaemia (p788)
 Rare in healthy people.
 Causes:decreased renal elimination (most
common), excessively rapid
administration, and movement of
potassium from ICF to ECF (Table 33.9).

 Signs & Symptoms: Slow heart rate,

ventricular fibrillation, paresthaesia.

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  Incorrectly
administered fluids
via IV can cause
hyperkalemia with
potentially fatal
consequences.

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 3. Electrolytes imbalances
Calcium
Hypocalcaemia (p793)
Causes:
1. Impaired bone mobilization
2. Increased losses from the kidneys
3. Increased protein binding
4. Soft tissue sequestration (acute pancreatitis)

Signs & Symptoms:

 Acute-
 Increased neuromuscular excitability (paresthaesia and
tetany), hypotension, cardiac dysrhythmias (Table
33.10).
 Chronic-
 Bone pain, deformities, fractures, skin dry and scaling,
nails brittle and hair dry. Cataracts is common.
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 4. Electrolytes imbalances
Calcium
Hypercalcaemia (p795)
 Causes: bone neoplasm and
hyperparathyroidism (Table 33.11).
Together 90% of reported cases. Others
such as excessive Vit. D supplements.
 Signs & Symptoms: Decreased neural
excitability (lethargy, weakness), increased
contractility of heart and dysrhythmias,
GIT effects (constipation, nausea,
vomiting, and anorexia), predisposition to
renal calculi, bone diseases.

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 There is a general mnemonic for remembering
the effects of hypercalcaemia: "groans
(constipation), moans (psychic moans (e.g.,
fatigue, lethargy, depression)), bones (bone
pain, especially if PTH is elevated), stones
(kidney stones), and psychiatric overtones
(including depression and confusion)."

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 5. Electrolytes imbalances
Phosphate
Hypophosphotaemia (p798)
 Causes: decreased intestinal absorption, increased
renal elimination, alcoholism.
 Signs & Symptoms:
 Altered neural function (weak), disturbed
musculoskeletal function (weakness), anaemia and
WBC dysfunction (Table 33.12).
Hyperphosphotaemia (p799)
 Causes: Impaired renal function (Table 33.13)
 Signs & Symptoms: related to calcium deficit.
Also increased soft tissue calcification in end-stage
renal disease.
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 6. Electrolytes imbalances
Magnesium
 Hypomagnesaemia (p801)
 Causes: impaired intake or absorption, increased
losses (Table 33.14)
 Signs & Symptoms:
 Usually occurs with hypocalcaemia and
hypokalaemia (diuretics). Neuromuscular irritability
and dysrhythmias.
 Hypermagnesaemia (p802)
 Causes: Decreased excretion (kidney disease), and
excessive intake (Table 33.13)
 Signs & Symptoms: Neuromuscular and
cardiovascular weaknesses.
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