Kidney Function & Disease
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 Bowman’s capsule
2. Bowman’s capsule:
– functions as a filter in the formation of
urine
3. Tubule composed of distinct segments:
– proximal tubule, descending and
ascending loop of Henle, distal tubule, and
collecting tubule (and collecting duct).
Efferent Arteriole
Proximal Tubule
Afferent
Arteriole
Distal Tubule
Glomerulus
Bowman’s
Capsule
Collecting
Duct
Loop of
Henle
peritubular
capillaries
Glomerular Filtration:
• Glomerular filtrate: the fluid that filters through the
glomerulus into Bowman’s Capsule, AKA glomerular
capsule (pressure of blood in the glomerulus causes fluid to
filter through the glomerular capillaries and into Bowman’s
Capsule).
• From there, blood flows into the proximal tubule  Loop of
Henle  distal tubule  collecting tubule  collecting
duct (which collects fluid from many nephrons)
• Collecting duct empties into the renal pelvis  ureters 
urinary bladder
• As glomerular filtrate flows through the tubules,
>99% of water and varying amounts of solutes are
reabsorbed into the peritubular capillaries
(capillaries that surround the tubule system).
• Substances are also secreted from peritubular
capillaries directly into the tubular fluid to be
excreted.
• The remaining water and solutes becomes urine.
Autoregulation of GFR: 2 Feedback
Mechanisms
GFR = Glomerular Filtration Rate:
The volume of blood plasma filtered out of the
glomeruli of both kidneys per minute. Normal
GFR = 90-120 ml/min Best estimate of kidney
function
(Note: GFR declines with age)
Age
Average GFR
20-29
116
30-39
107
40-49
99
50-59
93
60-69
85
70+
75
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
b. Secretes renin (enzyme), which converts Angiotensin I
to angiotensin II
c. Angiotensin II is a vasoconstrictor  increased BP
d. Angiotensin II also stimulates aldosterone secretion
e. Aldosterone increases Na+ and H2O reabsorption,
increased plasma volume, and increased BP
(aldosterone also stimulates potassium secretion into
tubules)
2. Produces erythropoietin
a. Stimulates erythropoiesis in bone marrow
b. The anemia of CRF is primarily caused by
impaired erythropoiesis
c.  RBC formation is mainly due to 
erythropoietin production in the diseased
kidneys, although other compounds that
accumulate in renal failure may also suppress
erythropoiesis.
3. Maintains Calcium-Phosphorus bone homeostasis
a.
Activates Vitamin D (Hydroxylation of 25-OH-D3 to
1,25-OH-D3) in kidney disease, can supplement
calcitriol, but very expensive Low vit. D  less Ca++
absorbed
b. Inverse relationship between Ca++ and P, so when P is
retained by diseased kidney, Ca++ levels decline (less
calcium reabsorbed by the kidney).
c. Low serum calcium  parathyroid gland releases PTH:
Parathyroid Hormone: works to elevate serum Ca++
by pulling it from the bones  fragility, muscular
weakness, decreased muscular tone, and general
neuromuscular hypoexcitability.
Kidney Disease
I.
Nephritic Syndrome: group of diseases
characterized by glomerular inflammation
(glomerulonephritis)
•
•
•
•
•
•
Hematuria, HTN, mild  in renal fx.
Caused by infection, SLE, other causes
Acute: either resolves or  nephrotic syndrome or
ESRD.
MNT: maintain good nutr. Status
(no restriction of prot/K+)
If HTN, restrict Na+
II. Nephrotic Syndrome:
symptoms resulting from
decreased glomerular function.
• Glomerular capillary permeability increases
markedly (and probably capillary permeability
throughout the body)
• Often an early sign of renal failure, especially in
diabetes.
A. Characterized by:
1. Proteinuria
(hallmark of nephrotic syndrome) – urinary
protein loss of >3g/day
(2’ increased capillary permeability)
a. Hypoalbuminemia
•
b. loss of immunoglobulins
•
c. loss of transferrin
•
d. loss of vitamin D binding protein
•
2. Edema 2’
3. Hyperlipidemia
•
•
4. Also possible:
• blood coagulation disorders or increased
clotting (can  occlusions in lungs and legs)
B. Possible causes:
1. SLE, glomerulonephritis
2. Infections
3. diabetes mellitus
4. drugs/toxins
5. lipid nephrosis (more rare, seen in kids)
lipid deposited in kidney tissue.
C. Nutrition Therapy
1. Energy:
2. High protein not recommended;
accelerates kidney failure. RDA is
appropriate.
3. Fat:
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. Uremia: azotemia plus the clinical signs
and symptoms of weakness, ill feeling,
n/v/d, itching (pruritis 2’ Ca, Na
deposition), muscle cramps, hiccups,
twitching, emotional irritability,  mental
capacity.
2. Proteinuria
3. Hyperkalemia (2’  clearance; nephropathy
can cause deficiency in or resistance to
aldosterone)
4. Sodium: sodium retention resulting in
fluid retention, HTN, edema, CHF.
– Some patients experience loss of high amounts
of sodium: salt losing enteropathy.
5. Hyperphosphatemia
6. Acid-base balance:  uric acid secretion and
bicarbonate production  metabolic
acidosis
7. Blood volume changes
a. Oliguric phase: very little urinary output
– blood pressure rises sharply. Can 
pulmonary edema (remember from HTN
chapter)
b. Diuretic phase: large losses of fluids and
electrolytes
c. Recovery phase: (hopefully) –
everything normalizes.
C. Treatment
1. Treat underlying disorder
2. Nutrition Therapy
a. High Energy 2’ hypermetabolism
–
–
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
www.kidney.org
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
c. Poss. GI ulceration and bleeding
d. Skin: may become yellowed. Urea from
sweat may crystallize on skin = uremic frost.
Pruritis (itching)
e. PEM 
f. HTN
g. Hypertriglyceridemia
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 patient’s 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