1B

Angela Putri
405090139
 Positions of
urinary organs
(posterior
view). Notice
that the
upper part of
the kidney
reaches the
level of the
margin of
pleura and
lung.
 Retroperitoneal organs, urinary
system in situ (anterior view). The
peritoneum has been
removed. Red = arteries; blue =
veins.
 Lymph
vessels and
lymph nodes
of the
posterior wall
of thoracic
and
abdominal
cavities
(anterior
aspect).
Green =lymph
vessels and
nodes; blue
=veins; red
=arteries;
white =
nerves.
 The kidneys
The kidneys lie retroperitoneally on the
posterior abdominal wall; the right
kidney is 0.5 in (12 mm) lower than the
left, presumably because of its
downward displacement by the bulk of the
liver. Each measures approximately
4.5 in (11 cm) long, 2.5 in (6 cm) wide and
1.5 in (4 cm) thick
 Posteriorlythe diaphragm (separating pleura), quadratus lumborum, psoas,
transversus abdominis, the 12th rib and three nervesthe subcostal (T12),
iliohypogastric and ilio-inguinal (L1).
Anteriorlythe right kidney is related to the liver, the 2nd part of the
duodenum (which may be opened accidentally in performing a right
nephrectomy), and the ascending colon. In front of the left kidney lie the
stomach, the pancreas and its vessels, the spleen, and the descending colon.
The suprarenals sit on each side as a cap on the kidneys upper pole.
The medial aspect of the kidney presents a deep vertical slit, the hilum, which
transmits, from before backwards, the renal vein, renal artery, pelvis of the ureter
and, usually, a subsidiary branch of the renal artery.
Lymphatics and nerves also enter the hilum, the latter being sympathetic, mainly
vasomotor, fibres.
The pelvis of the ureter is subject to considerable anatomical variations, it may
lie completely outside the substance of the kidney (even to the extent of having
part of the major calyces extrarenal) or may be almost buried in the renal hilum.
All gradations exist between these extremes. If a calculus is lodged in the pelvis
of the ureter, its removal is comparatively simple when this is extrarenal, and it is
correspondingly difficult when the pelvis is hidden within the substance of the
kidney.
Within the kidney, the pelvis of the ureter divides into two or three major calyces,
each of which divides into a number of minor calyces.
Each of these, in turn, is indented by a papilla of renal tissue and it is here that
the collecting tubules of the kidney discharge urine into the ureter.
The kidneys lie in an abundant fatty cushion (perinephric fat) contained in the
renal fascia (Fig. 83). Above, the renal fascia blends with the fascia over the
diaphragm, leaving a separate compartment for the suprarenal
 (which is thus easily separated and left behind in performing a
nephrectomy). Medially, the fascia blends with the sheaths of the
aorta and inferior vena cava. Laterally it is continuous with the
transversalis fascia. Only inferiorly does it remain relatively open
tracking around the ureter into the pelvis.
The kidney has, in fact, three capsules:
1fascial (renal fascia);
2fatty (perinephric fat);
3truethe fibrous capsule which strips readily from the normal
kidney surface but adheres firmly to an organ that has been
inflamed.

Blood supply
The renal artery derives directly from the aorta. The renal vein
drains directly into the inferior vena cava. The left renal vein passes
in front of the aorta immediately below the origin of the superior
mesenteric artery. The right renal artery passes behind the inferior
vena cava.

Lymph drainage
Lymphatics drain directly to the para-aortic lymph nodes.
 1Blood from a ruptured kidney or pus in a perinephric abscess first
distend the renal fascia, then force their way within the fascial
compartment downwards into the pelvis. The midline attachment of the
renal fascia prevents extravasation to the opposite side.

2In hypermobility of the kidney (floating kidney), this organ can be

moved up and down in its fascial compartment but not from side to side.
To a lesser degree, it is in this plane that the normal kidney moves during
respiration.

3Exposure of the kidney via the loin. An oblique incision is usually

favoured midway between the 12th rib and the iliac crest, extending
laterally from the lateral border of erector spinae. Latissimus dorsi and
serratus posterior inferior are divided and the free posterior border of
external oblique is identified, enabling this muscle to be split along its
fibres. Internal oblique and transversus abdominis are then divided,
revealing peritoneum anteriorly, which is pushed forward. The renal
fascial capsule is then brought clearly into view and is opened. The
subcostal nerve and vessels are usually encountered in the upper part of
the incision and are preserved. If more room is required, the lateral edge
of quadratus lumborum may be divided and also the 12th rib excised,
care being taken to push up, but not to open, the pleura, which crosses
the medial half of the rib.
 The ureter
The ureter is 10 in (25 cm) long and comprises the pelvis of the ureter (see above) and its
abdominal, pelvic and intravesical portions.

The abdominal ureter lies on the medial edge of psoas major (which separates it from the
tips of the transverse processes of L2L5) and then crosses into the pelvis at the
bifurcation of the common iliac artery in front of the sacroiliac joint. Anteriorly, the right
ureter is covered at its origin by the second part of the duodenum and then lies lateral to
the inferior vena cava and behind the posterior peritoneum. It is crossed by the testicular
(or ovarian), right colic, and ileocolic vessels. The left ureter is crossed by the testicular (or
ovarian) and left colic vessels and then passes above the pelvic brim, behind the
mesosigmoid and sigmoid colon to cross the common iliac artery immediately above its
bifurcation.

The pelvic ureter runs on the lateral wall of the pelvis in front of the internal iliac artery to
just in front of the ischial spine; it then turns forwards and medially to enter the bladder. In
the male it lies above the seminal vesicle near its termination and is crossed superficially
by the vas deferens (see Fig. 87). In the female, the ureter passes above the lateral fornix
of the vagina 0.5 in (12 mm) lateral to the supravaginal portion of the cervix and lies below
the broad ligament and uterine vessels (see Fig. 104).

The intravesical ureter passes obliquely through the wall of the bladder for 0.75 in (2 cm);
the vesical muscle and obliquity of this course produce respectively a sphincteric and
valve-like arrangement at the termination of this duct.

Blood supply
The ureter receives a rich segmental blood supply from all available arteries along its
course: the aorta, and the renal, testicular (or ovarian), internal iliac and inferior vesical
arteries.
1The ureter is readily identified in life by its thick muscular wall which is
seen to undergo worm-like (vermicular) writhing movements, particularly
if gently stroked or squeezed.
2Throughout its abdominal and the upper part of its pelvic course, it
adheres to the overlying peritoneum (through which it can be seen in the
thin subject), and this fact is used in exposing the ureter as the parietal
peritoneum is dissected upwards, the ureter comes into view sticking to its
posterior aspect.
3The ureter is relatively narrowed at three sites:
at the junction of the pelvis of ureter with its abdominal part,
at the pelvic brim, and
at the ureteric orifice (narrowest of all).
Aureteric calculus is likely to lodge at one of these three levels.
4In searching for a ureteric stone on a plain radiograph of the abdomen,
one must imagine the course of the ureter in relation to the bony skeleton
(Fig. 84). It lies along the tips of the transverse processes, crosses in front of
the sacroiliac joint, swings out to the ischial spine and then passes medially
to the bladder. An opaque shadow along this line is suspicious of calculus.
This course of the ureter is readily studied by examining a radiograph
 The embryology and congenital abnormalities
of the kidney and ureter (Fig. 85)
The kidney and ureter are mesodermal in origin and develop in an
unusual manner of considerable interest to the comparative
anatomist.
The pronephros, of importance in the lower vertebrates, is transient
in humans, but the distal part of its duct receives the tubules of the
next renal organ to develop, the mesonephros, and now becomes
the mesonephric or Wolffian duct.
The mesonephros itself then disappears except for some of its ducts
which form the efferent tubules of the testis. For further details of the
fates of the mesonephros and mesonephric duct, see page 148.
Adiverticulum then appears at the lower end of the mesonephric
duct which develops into the metanephric duct; on top of the latter a
cap of tissue differentiates to form the definitive kidney or
metanephros.
The metanephric duct develops into the ureter, pelvis, calyces and
collecting tubules, the metanephros into the glomeruli and the
proximal part of the renal duct system.
 Developmental abnormalities (Fig. 86)
1It is common for one or more distally placed arteries to persist (aberrant renal
arteries) and one may even run to the kidney from the common iliac artery.

2Occasionally the kidney will fail to migrate cranially, resulting in a persistent

pelvic kidney.

3The two metanephric masses may fuse in development, forming a horseshoe

kidney linked across the midline.

4In 1 in 2400 births there is complete failure of development of one kidney

(congenital absence of the kidney).

5Congenital polycystic kidneys (which are nearly always bilateral) are believed to
result from failure of metanephric tissue to link up with some of the metanephric duct
collecting tubules; blind ducts therefore form which subsequently become distended
with fluid. This theory of origin does not explain their occasional association with
multiple cysts of the liver, pancreas, lung and ovary.

6The mesonephric duct may give off a double metanephric bud so that two ureters
may develop on one or both sides. These ureters may fuse into a single duct
anywhere along their course or open separately into the bladder (where the upper
ureter enters below the lower ureter).

Rarely, the extra ureter may open ectopically into the vagina or urethra resulting in
urinary incontinence.
 The bladder (Figs 62, 63, 87)
The urinary bladder of a normal subject is uncomfortably distended by half a pint of fluid.
When fully distended, the adult bladder projects from the pelvic cavity into the abdomen,
stripping the peritoneum upwards from the anterior abdominal wall. The surgeon utilizes
this fact in carrying out an extraperitoneal incision or suprapubic puncture into the bladder.
In children up to the age of about 3 years, the pelvis is relatively small and the bladder is,
in fact, intra-abdominal although still extraperitoneal.

Relations
Anteriorlythe pubic symphysis.
Superiorly the bladder is covered by peritoneum with coils of small intestine and
sigmoid colon lying against it. In the female, the body of the uterus flops against its
posterosuperior aspect.
Posteriorlyin the male the rectum, the termination of the vasa deferentia and the
seminal vesicles; in the female, the vagina and the supravaginal part of the cervix.
Laterallythe levator ani and obturator internus.

The neck of the bladder fuses with the prostate in the male; in the female it lies directly on
the pelvic fascia surrounding the short urethra.
The muscle coat of bladder is formed by a criss-cross arrangement of bundles; when
these undergo hypertrophy in chronic obstruction (due to an enlarged prostate, for
example) they account for the typical trabeculated open weave appearance of the
bladder wall, readily seen through a cystoscope.
The circular component of the muscle coat condenses as an (involuntary) internal urethral
sphincter around the internal orifice. This can be destroyed without incontinence providing
the external sphincter remains intact (as occurs in prostatectomy).
 Cystoscopy
The interior of the bladder and its three orifices (the internal meatus and the two ureters)
are easily inspected by means of a cystoscope. The ureteric orifices lie 1 in (2.5 cm) apart
in the empty bladder, but when this is distended for cystoscopic examination, the distance
increases to 2 in (5 cm).
The submucosa and mucosa of most of the bladder are only loosely adherent to the
underlying muscle and are thrown into folds when the bladder is empty, smoothing out
during distension of the organ. Over the trigone, the triangular area bounded by the
ureteric orifices and the internal meatus, the mucosa is adherent and remains smooth
even in the empty bladder.
Between the ureters, a raised fold of mucosa can be seen called the interureteric ridge
which is produced by an underlying bar of muscle.
Blood supply
Blood is supplied from the superior and inferior vesical branches of the internal iliac artery.
The vesical veins form a plexus which drains into the internal iliac vein.
Lymph drainage
Lymphatics drain alongside the vesical blood vessels to the iliac and then para-aortic
nodes.
Nerve supply
Efferent parasympathetic fibres from S2 to S4 accompany the vesical arteries to the
bladder. They convey motor fibres to the muscles of the bladder wall and inhibitory fibres
to its internal sphincter. Sympathetic efferent fibres are said to be inhibitory to the bladder
muscles and motor to its sphincter, although they may be mainly vasomotor in function, so
that normal filling and emptying of the bladder are probably controlled exclusively by its
parasympathetic innervation. The external sphincter is made up of striated muscle. It is
also concerned in the control of micturition and is supplied by the pudendal nerve (S2, 3,
4). Sensory fibres from the bladder, which are stimulated by distension, are conveyed in
both the sympathetic and parasympathetic nerves, the latter pathway being the more
important.
 The urethra
The male urethra (Fig. 87b)
The male urethra is 8 in (20 cm) long and is divided into the prostatic, membranous and
spongy parts.
The prostatic urethra (1.25 in (3 cm)), as its name implies, traverses the prostate. Its posterior
wall bears a longitudinal elevation termed the urethral crest, on each side of which is a shallow
depression, the prostatic sinus, into which the 1520 prostatic ducts empty. At about the
middle of the crest is a prominence termed the colliculus seminalis (verumontanum) into which
opens the prostatic utricle. This is a blind tract, about 5mm long, running downwards from the
substance of the median lobe of the prostate. It is believed to represent the male equivalent of
the vagina, a remnant of the paramesonephric duct (see page 148). On either side of the
orifice of the prostatic utricle open the ejaculatory ducts, formed by the union of the duct of the
seminal vesicle and the terminal part of the vas deferens.
The membranous urethra (0.75 in (2 cm)) pierces the external sphincter urethrae (the
voluntary sphincter of the bladder) and the fascial perineal membrane which covers the
superficial aspect of the sphincter.
The spongy urethra (6 in (15 cm)) traverses the corpus spongiosum of the penis. It first passes
upwards and forwards to lie below the pubic symphysis and then in its flaccid state bends
downwards and forwards.

1Where the urethra passes beneath the pubis is a common site for it to be ruptured by a fall
astride a sharp object, which crushes it against the edge of the symphysis.

2The external orifice is the narrowest part of the urethra and a calculus may lodge there.
Immediately within the meatus, the urethra dilates into a terminal fossa whose roof bears a
mucosal fold (the lacuna magna) which may catch the tip of a catheter. Instruments should
always be introduced into the urethra beak downwards for this reason.
 The female urethra
The female urethra is 1.5 in (4 cm) long; it traverses the sphincter urethrae and lies
immediately in front of, indeed embedded in the wall of, the vagina. Its external
meatus opens 1 in (2.5 cm) behind the clitoris. The sphincter urethrae in the female is
a tenuous structure and vesical control appears to depend mainly on the intrinsic
sphincter of condensed circular muscle fibres of the bladder.

The mucosa of the urinary tract

The pelvis, ureter, bladder and urethra are lined by a transitional epithelium as far as
the entry of the ejaculatory ducts in the prostatic urethra. This is conveniently termed
the uroepithelium since it has a uniform appearance and is subject to the same
pathological processes for example, the development of papillomata. The
remainder of the urethra has a columnar lining except at its termination, where the
epithelium becomes squamous.

Radiology of the urinary tract

The renal contours can often be identified on a soft tissue radiograph of the
abdomen. Intravenous injection of iodine-containing compounds excreted by the
kidney will produce an outline of the calyces and the ureter (intravenous urogram).
When the injection medium enters the bladder, a cystogram is obtained
Further information can be obtained by passing a catheter up the ureter through a
cystoscope and injecting radio-opaque fluid to fill the pelvis and calyx system
(retrograde pyelogram). Similarly, injection of such fluid into the urethra or bladder
may be used for the radiographic study of these viscera.
The kidneys are beautifully delineated in transverse section on CT scans
 OVERVIEW OF KIDNEY FUNCTIONS
1. Maintaining H2O balance in the body
2. Maintaining the proper osmolarity of body fl uids, primarily through regulating H2O
balance. Th is function is important to prevent osmotic fl uxes into or out of the cells,
which could lead to detrimental swelling or shrinking of the cells, respectively
3. Regulating the quantity and concentration of most ECF ions,including sodium (Na),
chloride (Cl), potassium (K), calcium (Ca2), hydrogen ion (H), bicarbonate (HCO3 ),
phosphate (PO4 3), sulfate (SO4 2), and magnesium (Mg2). Even minor fl uctuations
in the ECF concentrations of some of these electrolytes can have profound infl
uences. For example, changes in the ECF concentration of K can potentially lead to
fatal cardiac dysfunction.
4. Maintaining proper plasma volume, which is important in the long-term regulation
of arterial blood pressure. Th is function is accomplished through the kidneys
regulatory role in salt (Na and Cl) and H2O balance (Chapter 15).
5. Helping maintain the proper acidbase balance of the body by adjusting urinary
output of H and HCO3
6. Excreting (eliminating) the end products (wastes) of bodily metabolism, such as
urea (from proteins), uric acid (from nucleic acids), creatinine (from muscle creatine),
bilirubin (from hemoglobin), and hormone metabolites. If allowed to accumulate,
many of these wastes are toxic, especially to the brain.
7. Excreting many foreign compounds, such as drugs, food additives, pesticides, and
other exogenous nonnutritive materials that have entered the body.
8. Producing erythropoietin, a hormone that stimulates red blood cell production
9. Producing renin, an enzymatic hormone that triggers a chain reaction important in
salt conservation by the kidneys.
10. Converting vitamin D into its active form
 TRANSEPITHELIAL TRANSPORT To be reabsorbed, a substance must traverse fi ve distinct barriers:
It must leave the tubular fl uid by crossing the luminal membrane of the tubular cell ( Figure 14-14,
step 1).
It must pass through the cytosol from one side of the tubular cell to the other (step 2 ).
It must cross the basolateral membrane of the tubular cell to enter the interstitial fl uid (step 3 ).
It must diff use through the interstitial fl uid (step 4 ).
It must penetrate the capillary wall to enter the blood plasma (step 5 ).
This entire sequence of steps is known as transepithelial (across the epithelium) transport.
 Acute Renal Failure
Acute renal failure (ARF) is characterized by a
rapid decline in glomerular filtration rate (GFR)
over hours to days.
ARF complicates approximately 57% of hospital
admissions and up to 30% of admissions to intensive
care units.
Retention of nitrogenous waste products, oliguria
(urine output <400 mL/d contributing to extracellular
fluid overload), and electrolyte and acid-base
abnormalities are frequent clinical features.
 Epidemiology
Incidence in the United States
Approximately 1% of patients admitted to hospitals have acute
kidney injury (AKI) at the time of admission. The estimated
incidence rate of AKI is 2-5% during hospitalization.
AKI develops within 30 days postoperatively in approximately
1% of general surgery cases ; it develops in up to 67% of
intensive care unit (ICU) patients. Approximately 95% of
consultations with nephrologists are related to AKI.
Feest and colleagues calculated that the appropriate
nephrologist referral rate is approximately 70 cases per million
population.
Race predilection
No race predilection is recognized in AKI.
Sex predilection
Males and females are affected equally by AKI.
 Categories of AKI

AKI may be classified into 3 general

categories, as follows:
Prerenal - as an adaptive response to severe
volume depletion and hypotension, with
structurally intact nephrons
Intrinsic - in response to cytotoxic, ischemic,
or inflammatory insults to the kidney, with
structural and functional damage
Postrenal - from obstruction to the passage of
urine
Four phases of acute tubular necrosis.
 Urinalysis
Anuria suggests complete urinary tract obstruction but may complicate severe cases of
prerenal or intrinsic renal ARF.
In prerenal ARF, the sediment is characteristically acellular and contains transparent
hyaline casts ("bland," "benign," "inactive" urine sediment).
Hyaline casts
Postrenal ARF may also present with an inactive sediment,
hematuria and pyuria are common in patients with intraluminal obstruction or prostatic
disease.
Pigmented "muddy brown" granular casts and casts containing tubule epithelial cells are
characteristic of ATN and suggest an ischemic or nephrotoxic etiology.
These casts are usually found in association with mild "tubular" proteinuria (<1 g/d),
reflecting impaired reabsorption and processing of filtered proteins by injured proximal
tubules.
broad granular casts are characteristic of chronic kidney disease and probably reflect
interstitial fibrosis and dilatation of tubules.
Eosinophiluria (>5% of urine leukocytes) is a common finding (~90%) in antibiotic-induced
allergic interstitial nephritis and can be detected with Hansel's stain;
lymphocytes may predominate in allergic interstitial nephritis induced by NSAIDs and some
other drugs (i.e., ampicillin, rifampicin, and interferon ).
uric acid crystals (pleomorphic in shape) are common in the concentrated urine of prerenal
ARF but suggest acute urate nephropathy if seen in abundance.
Oxalate (envelope-shaped) and hippurate (needle-shaped) crystals raise the possibility of
ethylene glycol ingestion and toxicity.
Proteinuria of >1 g/d suggests injury to the glomerular ultrafiltration barrier ("glomerular
proteinuria") or excretion of myeloma light chains.
Hemoglobinuria or myoglobinuria should be suspected if urine is strongly positive for heme
by dipstick but contains few red cells, and if the supernatant of centrifuged urine is positive
for free heme.
Bilirubinuria may provide a clue to the presence of HRS.
 Renal Failure Indices
Analysis of urine and blood biochemistry
distinguishing prerenal ARF from ischemic or
nephrotoxic intrinsic renal ARF.
The fractional excretion of sodium (FENa)
high in ischemic ATN
low in patients with sepsis-induced, pigment-
induced, and some forms of nephrotoxic ATN (e.g.,
contrast-associated). In contrast, creatinine is not
reabsorbed in either setting.
The FENa may be >1.0% in prerenal ARF if
patients are receiving diuretics or with
preexisting chronic kidney disease, certain
salt-wasting syndromes, or adrenal
insufficiency.
 Laboratory Findings
Serial serum creatinine
Creatinine rises rapidly (within 2448 h) in patients with ARF following renal
ischemia, atheroembolization, and radiocontrast exposure.
Peak serum creatinine concentrations are observed after 35 days with contrast
nephropathy and return to baseline after 57 days
serum creatinine concentrations typically peak later (710 days) in ATN and
atheroembolic disease.
The initial rise in serum creatinine is characteristically delayed until the second
week of therapy with many tubular epithelial cell toxins (e.g., aminoglycosides,
cisplatin) and is thought to reflect the need for accumulation of these agents
within tubular epithelial cells to cause injury.
Hyperkalemia, hyperphosphatemia, hypocalcemia, and elevations in serum
uric acid and creatine kinase (MM isoenzyme) levels rhabdomyolysis.
Hyperuricemia [>890 mol/L (>15 mg/dL)] , hyperkalemia,
hyperphosphatemia, and increased circulating levels of intracellular
enzymes ( lactate dehydrogenase) acute urate nephropathy and tumor
lysis syndrome following cancer chemotherapy.
A wide anion and osmolal gap unusual anion or osmole in the circulation
(e.g., ingestion of ethylene glycol or methanol).
Severe anemia in the absence of hemorrhage hemolysis, multiple
myeloma, or thrombotic microangiopathy.
Systemic eosinophilia allergic interstitial nephritis// atheroembolic disease
and polyarteritis nodosa.
 Radiologic Findings
ultrasonography exclude postrenal ARF.
CT and MRI, CT-based angiography, Doppler ultrasound,
alternative imaging modalities.
Retrograde or anterograde pyelography more definitive
investigations in complex cases and provide precise localization
of the site of obstruction.
A plain film of the abdomen or unenhanced helical CT scan
initial screening technique suspected nephrolithiasis.
Magnetic resonance angiography (MRA) patency of renal
arteries and veins suspected vascular obstruction.
Catheter-based angiography definitive diagnosis and treatment.
Renal Biopsy
prerenal and postrenal ARF have been excluded and the cause
of intrinsic ARF is unclear.
clinical assessment and laboratory investigations suggest
diagnoses other than ischemic or nephrotoxic injury that may
respond to disease-specific therapy.
Examples include glomerulonephritis, vasculitis, and allergic
interstitial nephritis.
 Complications
Expansion of extracellular fluid volume
Hyperkalemia
metabolic acidosis
Hyperphosphatemia
Anemia
Infection
Cardiopulmonary complications
uremic syndrome
A vigorous diuresis
Hypernatremia
Hypokalemia , hypomagnesemia , hypophosphatemia, and
hypocalcemia develop in response to injury associated with
selected drugs (e.g., ifosphamide may lead to Fanconi syndrome or
type II renal tubular acidosis associated with hypokalemia, acidosis,
hypophosphatemia, and glycosuria).
 Treatment
Maintenance of Volume Homeostasis and Correction of Biochemical Abnormalities
Furosemide (IV) doses.
all medications cleared by renal excretion should be avoided or their doses should be adjusted
appropriately.
Correcting Severe Acidosis
bicarbonate administration
Therapeutic agents, such as dopamine, nesiritide, fenoldopam, and mannitol, are not indicated in
the management of AKI and may be harmful for the patient.
Treatment of Hyperkalemia
decreasing the intake of potassium in diet or tube feeds,
exchanging potassium across the gut lumen using potassium-binding resins,
promoting intracellular shifts in potassium with insulin and dextrose solutions,
instituting dialysis.
Correcting Hematologic Abnormalities
(eg, anemia, uremic platelet dysfunction) transfusions and administration of desmopressin or
estrogens.
Dietary Modification
Salt and fluid restriction
In the polyuric phase of AKI, potassium and phosphorus may be depleted, and patients require
dietary supplementation and intravenous replacement.
Calculation of the nitrogen balance
Critically ill patients should receive at least 1 g/kg/d protein intake but should avoid
hyperalimentation, which can lead to an elevated BUN level and water loss resulting in
hypernatremia.
 Long-Term Monitoring

Renal recovery is usually observed within

the first 2 weeks, and many nephrologists
tend to diagnose patients with end-stage
(ie, irreversible) renal failure 6-8 weeks
after the onset of acute kidney injury (AKI).
It is always better to check these patients
periodically, because some patients may
regain renal function much later.
 Chronic Kidney Disease
encompasses a spectrum of different
pathophysiologic processes associated
with abnormal kidney function, and a
progressive decline in glomerular filtration
rate (GFR).
chronic renal failure applies to the process
of continuing significant irreversible
reduction in nephron number, and typically
corresponds to CKD stages 35.
 aWith risk factors for CKD
bWith demonstrated kidney damage (e.g., persistent proteinuria, abnormal urine sediment,
abnormal blood and urine chemistry, abnormal imaging studies).
 Etiology and Epidemiology
at least 6% of the adult population in the United States has chronic kidney
disease at stages 1 and 2.
An additional 4.5% of the U.S. population is estimated to have stages 3
and 4 CKD.
The most frequent cause of CKD is diabetic nephropathy
Hypertensive nephropathy is a common cause of CKD in the elderly, in
whom chronic renal ischemia as a result of small and large vessel
renovascular disease may be underrecognized.
Progressive nephrosclerosis from vascular disease is the renal correlate
of the same processes that lead to coronary heart disease and
cerebrovascular disease.
The early stage of CKD, manifesting as albuminuria and even a minor
decrement in GFR, is now recognized as a major risk factor for
cardiovascular disease.
The striking interindividual variability in the rate of progression to CKD has
an important heritable component
women of reproductive age are relatively protected against progression of
many renal diseases, and sex-specific responses to angiotensin II and its
blockade have been identified.
 Pathophysiology
(1) initiating mechanisms specific to the underlying etiology
(e.g., immune complexes and mediators of inflammation
in certain types of glomerulonephritis, or toxin exposure
in certain diseases of the renal tubules and interstitium);
(2) a set of progressive mechanisms,
underlying etiology
long-term reduction of renal mass
hyperfiltration and hypertrophy of the remaining viable
nephrons
increased pressure and flow predisposes to sclerosis
and dropout of the remaining nephrons
maladaptive hypertrophy and sclerosis
FIGURE 115-1 Common symptoms and signs of chronic renal failure.
 NEPHROTIC SYNDROME
albuminuria in amounts of more than 3
-3.5 g/day +++ hypoalbuminemia, edema,
and hyperlipidemia.
 Idiopathic Nephrotic Syndrome
Minimal Change Disease
nephrotic syndrome in children
A similar histologic pattern may be seen as an adverse reaction to
certain medications (nonsteroidal anti-inflammatory drugs [NSAIDs],
lithium) and in association with certain tumors (Hodgkin's disease
and leukemias).
weight gain and periorbital and peripheral edema related to the
proteinuria, which is usually well into the nephrotic range.
Additional findings in adults are hypertension and microscopic
hematuria
active urinary sediment with erythrocyte casts is not found.
Many adult patients have mild to moderate azotemia, which may be
related to hypoalbuminemia and intravascular volume depletion.
Complement levels and serologic test results are normal.
 Focal Segmental Glomerulosclerosis
found on biopsy
most common form of idiopathic nephrotic syndrome in blacks.
FSGS may be either idiopathic or secondary to a number of different causes (e.g.,
heroin abuse, HIV infection, sickle cell disease, obesity, reflux of urine from the
bladder to the kidneys, and lesions associated with a single or remnant kidneys).
result of genetic defects in structural components of the visceral epithelial cell.
autosomal recessive pattern of nephrotic syndrome secondary to mutations in the
structural protein podocin
autosomal dominant mutations in the structural protein -actinin 4, as well as in the
TRCP6 glomerular slit diaphragmassociated channel.
In general, such patients with genetic forms of the disease are steroid resistant,
have a progressive course, and do not experience recurrences of FSGS when
they receive a renal transplant.
asymptomatic proteinuria or edema.
Hypertension is found in 30 to 50%,
microscopic hematuria
glomerular filtration rate (GFR) is decreased
Complement levels and other serologic test results are normal.
By LM, initially only some glomeruli have areas of segmental scarring glomeruli
with segmental sclerosing lesions and increased numbers of globally sclerotic
glomeruli.
By IF staining, IgM and C3 are commonly trapped in the areas of glomerular
sclerosis.
EM shows no deposits and only effacement of visceral epithelial cell foot
processes.
variants of FSGS benign course and prognosis (e.g., the tip lesion variant) or a
more progressive course (e.g., the collapsing variant).
 Membranous Nephropathy
in white Americans.
associated with
infections (syphilis, hepatitis B and C),
systemic lupus erythematosus (SLE),
certain medications (gold salts, NSAIDs), and
certain tumors (solid tumors and lymphomas).
proteinuria and edema.
Hypertension and microhematuria are not infrequent findings
renal function and GFR are usually normal at diagnosis.
Despite the finding of complement in the glomerular immune
deposits, serum complement levels are normal.
associated with a hypercoagulable state and renal vein
thrombosis. (renal vein thrombosis and pulmonary emboli.)
sudden flank pain,
deterioration of renal function,
symptoms of pulmonary disease
 Membranoproliferative Glomerulonephritis
Idiopathic type I membranoproliferative or mesangiocapillary
glomerulonephritis (MPGN)
uncommon primary glomerular disease
association with certain infectious agents (hepatitis C), autoimmune
disease (SLE), and diseases of intraglomerular coagulation.
All of these stimuli have been proposed to incite the glomerular
mesangial cells to grow out along the capillary wall and split the GBM.
Type II MPGN, or dense deposit disease,
an even less common disease than MPGN type I,
associated with uncontrolled systemic activation of the alternative
complement pathway.
In most patients it is due to C3 nephritic factor
may be associated with partial lipodystrophy.
Most patients with idiopathic MPGN are children or young adults
proteinuria
A low serum complement level is found intermittently in type I MPGN
C3 level is always reduced in type II MPGN (dense deposit disease).
Prognosis: half the patients progressing to ESRD within 10 years of
diagnosis.
treat MPGN corticosteroids and other immunosuppressive
medications, as well as anticoagulants and antiplatelet agents.
Table 45-1 Initial Clinical and Laboratory Data Base for Defining Major
Syndromes in Nephrology
 Oliguria
refers to a 24-h urine output of <500 mL
cause of acute renal failure and carries a more serious
prognosis for renal recovery in all conditions except prerenal
azotemia.
anuria
is the complete absence of urine formation (<50 mL).
caused by total urinary tract obstruction, total renal artery or vein
occlusion, and shock (manifested by severe hypotension and
intense renal vasoconstriction).
Cortical necrosis, ATN, and rapidly progressive
glomerulonephritis can occasionally cause anuria.
Nonoliguria
urine output >500 mL/d in patients with acute or chronic
azotemia.
With nonoliguric ATN, disturbances of potassium and hydrogen
balance are less severe than in oliguric patients, and recovery to
normal renal function is usually more rapid.