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NFSC 370
McCafferty
Structure
Nephron:
functional unit of the kidney. Each
kidney has over a million nephrons.
Composed of:
1. Glomerulus filtering unit
network of capillaries originating from the
afferent arteriole
surrounded by Bowmans capsule
2. Bowmans capsule:
functions as a filter in the formation of
urine
Afferent
Arteriole
Distal Tubule
Glomerulus
Bowmans Collecting
Capsule Duct
peritubular
Loop of capillaries
Henle
Glomerular Filtration:
Glomerular filtrate: the fluid that filters through the
glomerulus into Bowmans Capsule, AKA glomerular
capsule (pressure of blood in the glomerulus causes fluid to
filter through the glomerular capillaries and into Bowmans
Capsule).
www.kidney.org/K/DOQI
1. If GFR drops, afferent arteriole dilates
to increase glomerular blood flow and
increase pressure, thereby increasing
GFR
2. If GFR drops, renin is released
resulting in the conversion of
angiotensin I to II. The efferent
arteriole constricts, increasing
glomerular pressure, and increasing
GFR.
Functions of the Kidneys
A. Homeostatic Functions
1. Waste excretion (urine formation)
a. Nitrogenous end products: urea, creatinine, uric acid,
etc.
b. Metabolic degradation of peptide hormones: glucagon,
insulin, PTH, growth hormone, FSH, and gastrin.
2. Fluid/electrolyte balance (Na+, K+, water)
3. Acid/base regulation:
kidneys generate and reclaim filtered bicarbonate, as well
as secrete excess acid to maintain balance.
4. Balance of other electrolytes (Ca++, Mg++,
Phosphate PO4 3-)
B. Non-excretory functions
1. Renin-angiotensin mechanism to control BP
a. Kidney senses decreased BP
4. Sodium:
III. Acute Renal Failure (ARF):
Sudden drop in GFR. Can develop in a
previously healthy person, and last from a few
days to several weeks.
A. Causes
1. Prerenal: sudden drop in blood volume or
renal bloodflow due to severe dehydration,
shock or trauma.
2. Intrinsic: damage to kidney cells 2
sustained shock, trauma, surgery,
septicemia, nephrotoxic agents, acute
glomerulonephritis.
3. Postrenal: (obstructive) Kidneys can form
urine, but excretion is impeded.
B. Consequences
1. Uremic Syndrome:
a. Azotemia: accumulation of nitrogenous
metabolites in the blood:
b. Protein: depends on renal function
No dialysis:
Dialysis:
c. Fluid: restricted to urinary output + 500 ml for insensible
losses (losses via lungs and skin). Increase if v/d/fever
d. Potassium:
e. Sodium:
3. Drugs
a. Diuretics during oliguric phase
b. Exchange resins: cause Na+ to be exchanged for K+ in
the colon so K+ is excreted.
c. Insulin: DM, and moves K+ into cells w/glucose
IV. Chronic Kidney Disease (CKD,
previouslyCRF):
Irreversible, progressive destruction of
nephrons. Leads to End Stage Renal Disease
(ESRD) .
A. Causes
1. ARF
2. Nephritis, renal artery obstruction, kidney
stones, nephrotic syndrome, polycystic
kidney disease
3. Diabetic nephropathy
4. HTN, atherosclerosis
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B. Progression
1. Magnification Phenomenon: As GFR falls,
function of remaining nephrons (adaptive
hypertrophy)
This is why it can go undetected. At Stage I: Protein
restriction and conservative management can slow
progression to ESRD. Control HTH and DM.
2. Kidney damage with normal or GFR
a. renal reserve, but asymptomatic
b. BUN, lytes,fluid balance, P, Ca++ ALL
NORMAL
3. Renal Insufficiency
a. Mild azotemia (mildly increased BUN, creat)
b. Impaired concentration of urine: urine
output is probably OK at this point, but
because concentrating ability is impaired, we
see nocturia
c. Mild anemia
d. Fatigue and decreased mental acuity
e. Challenges will accelerate renal deterioration
(ie. excessive protein load, P load, or
uncontrolled HTN, DM, etc.)
4. Frank Renal Failure
a. Anemia (normochromic normocytic, but low
Hgb/Hct)
b. Uremia
h. Hypocalcemia
i. Hyperphosphatemia, poss. hyperkalemia
j. Metabolic Acidosis
k. Fixed urinary output
l. Edema
m. Altered bone metabolism - Renal
osteodystrophy
5. ESRD End-Stage Renal Disease: GFR <20% of
normal
a. Uremia
b. Kidney replacement therapy required (dialysis
or transplant)
c. Others: hyperchloremia, hypermagnesemia,
hyperuricemia
V. Treatment of CKD
Goal: delay progression of renal failure, prevent
buildup of toxic metabolites, maintain or improve
nutrition status, control symptoms.
A. Diet (see handout)
B. Hemodialysis (HD)
Method of purifying the blood in
patients w/renal failure (GFR 4-5
ml/min). Takes over 2 main kidney
functions:
Waste removal
Fluid removal
The two major forms of dialysis are hemodialysis and peritoneal
dialysis. In hemodialysis, the patients blood is sent through a
machine that filters away waste products. The clean blood is
returned to the body. Hemodialysis is usually performed at a
dialysis center three times per week for 3 to 4 hours.
In peritoneal dialysis, a fluid (the dialysate) is dripped into the abdomen.
The dialysate captures the waste products from the blood, and after a few
hours is drained away. Then, a fresh bag of dialysate is used. Patients
using continuous ambulatory peritoneal dialysis (CAPD), the most
common form of peritoneal dialysis, change dialysate four times a day.
Another form of peritoneal dialysis, however, can be performed at night
with a machine that drains and refills the abdomen automatically. Patients
can perform peritoneal dialysis themselves.
VI. Consequences of CKD
Osteodystrophies:
1. P retention leads to serum Ca++ with PTH
secretion. Results in Ca++ being removed from
bones. Also in renal failure: intestinal absorption
of Ca++
2. Tendency toward spontaneous fractures, painful
joints, bone pain, metastatc calcification.
Cardiovascular Disease
1. Atherosclerosis: accelerated in CRF. TG, esp
w/HD
2. HTN due to Na+ and fluid retention, as well as
alteration in renin-angiotensin mechanism
3. Pericarditis: etiology unknown
Hematologic abnormalities: :
1. Anemia is almost universal
2. EPO, Fe Cardiovascular Disease
GI disorders:
Loss of appetite, n/v, may also see changes in GI
motility and absorption; GI hemorrhage
Neuropathy:
1. CNS manifestations: fatigue, insomnia,
depression, agitation; also convulsions, coma, and
death
2. dialysis dementia, related to aluminum