3.

1
04 Nov
2014

Renal Symptoms
Alfredo Guzman, M.D.
Wag mong hanapin sa butas ng donut ang sarap
Ron Capinding

PAUNAWA
Paulo Coelho
Ang trans na ito ay hango mula sa MED Trans ng 2B and 2D 2016 at
mula sa librong Harrisons 18th ed. May ilang mga notes na kasama
ito base sa mga napagusapan sa klase.

REVIEW OF ANATOMY
GROSS ANATOMY
Bean-shaped
Divided into 2 parts
o Cortex (outer portion); contains all the glomeruli
o Medulla (inner portion)
*Tubules are located in both the cortex and the medulla

MICROSCOPIC ANATOMY
NEPHRON
o Basic unit of the kidney
o Each nephron is composed of a tuft of capillaries called the
glomerulus
Glomerulus lies between the 2 arterioles (efferent and afferent)
After the glomerulus series of tubules , the length of which depends
on where the glomerulus is located

4.

Regulation of red cell mass by erythropoietin production

o Renal Failure
can lead to anemia d/t
erythropoietin
uremic toxins in RBC

CLINICAL MANIFESTATIONS OF RENAL DISEASES

1. Glomerular
2. Tubular
3. Interstitial
4. Vascular
FROM 2B 2016
Clinical manifestations of these disorders depends on
pathophysiology of the renal injury
Nephrologic syndromes usually consist of several elements
reflect the underlying pathologic processes
Duration and severity of the disease will affect these findings
typically include one or more of the following:
o disturbances in urine volume (oliguria, anuria, polyuria)
o abnormalities of urine sediment (RBCs, WBCs, casts,
crystals)
o abnormal excretion of serum proteins (proteinuria)
o reduction in GFR (azotemia)
o presence of hypertension and/or expanded total body
volume (edema)
o electrolyte abnormalities
o in some syndromes, fever/pain

the
that
and

and

fluid

AZOTEMIA
elevation of water-soluble metabolites in blood
retention of nitrogenous waste products (creatinine, urea) d/t reduced
GFR
results from:
o
reduced renal perfusion
o
intrinsic renal disease
o
postrenal processes (ureteral obstruction)
no associated symptoms
GFR
serum creatinine is the most widely used marker for GFR
directly proportional to urine creatinine excretion and inversely to
serum creatinine (UCR/PCR)
Urea
not constant
reabsorbed by the tubule

Azotemia
Elevation of water soluble
metabolites in the blood
Not associated with symptoms

1.
2.
3.

FUNCTIONS OF THE KIDNEY

Regulation of the composition and volume of body fluid
(Obligate H2O loss = 500mL/day)
Aid in the control of systemic blood pressure
Bio-activation of vitamin D3

implication: Calcium Metabolism

o Vit D3
aids in calcium absorption
D3 serum Ca level PTH Ca and PO4
Renal Osteodystrophy bone demineralization d/t
chronic renal disease

TRANSCRIBED BY: LUKE, LEIA, HAN, CHEWBACCA

Uremia
Same as above but with
associated symptoms
First Sx: Sleep disturbances

SERUM CREATINE
More reliable index of glomerular filtration rate (GFR) than urea
because of the latter's lower back-diffusion from tubule lumen to
peritubular blood
Mainly derived from metabolism of creatine or creatine
phosphokinase from skeletal muscle cells
Produced in almost constant rate
Steady state concentration dependent on renal excretion w/c
mainly reflects of GFR

APPROACH TO THE PATIENT: AZOTEMIA

decide if reduced GFR represents acute or chronic renal injury
clinical situation, history, and laboratory data helps in diagnosing
REDUCED SINGLE NEPHRON GLOMERULAR FILTRATION RATE
TUBULAR FUNCTION NORMAL
Tubular function is still intact
o volume of urine should not be below the obligate urine volume
loss
o ability of the kidneys to concentrate the urine is still intact
o the specific gravity should be elevated
o osmolarity should be high

Page 1 of 6

Renal Symptoms
Nov. 4, 2013

o urine sodium level should be low

o urine acidity there is some form of acidosis

such as:
o Glomerulonephritis
o Diabetic glomerulosclerosis

if that is not the case: there is a problem in tubular function: Acute

Tubular Necrosis/ Acute Renal Failure
PRE-RENAL AZOTEMIA
single nephron GFR
(SNGFR)
GFR of all single nephron is
reduced
Normal tubular function
Normal BUN: serum creatinine
concentration is 10:1
Elevated ratio also can be
produced by the following
factors:
o Tetracycline administration
o Glucocorticoid therapy
o Presence of blood in the
gastrointestinal tract
o Increased protein turnover
due to trauma or burn

POST-RENAL AZOTEMIA
Applied when acute
obstruction lowers single
nephron GFR (SNGFR)
causes azotemia
Causes backflow
Increased pressure
Compression
Renal injury
Acute incomplete
obstruction of the ureter and
acute glomerular injury also
may reduce SNGFR and leave
tubule function relatively
intact

*Diminished nephron number by 75% = pt. will be

dependent on DIALYSIS
Decreased

In patients with chronic renal disease

o Total GFR is sufficient to support life only
because of a very high SNGFR
o Inadvertent dehydration or any other factor
that lowers the SNGFR provoke oliguria
and severe azotemia
This is acute renal failure on top of chronic renal
disease!
o mabilis magkaroon ng UREMIA

Oliguria

TUBULAR FUNCTION IMPAIRED

Anuria
ACUTE RENAL FAILURE

Certain acute renal diseases that produce azotemia

Lower single nephron GFR (SNGFR) and damage the

tubules sufficiently

Reduce or even abolish tubules reabsorptive function

Produce acute renal failure

Nonoliguria

OLIGURIA AND ANURIA

24h urine output of 400 ml or less
can accompany any cause of acute RF
serious prognosis for renal recovery in all
conditions except prerenal azotemia
urine volume of 40 ml or less
complete absence of urine formation
(<100mL Harrisons 18th Ed.)
caused by:
o total urinary tract obstruction
o total renal artery or vein occlusion
o shock (severe hypotension and intense
renal vasoconstriction)
o cortical necrosis
o ATN
o Rapidly progressive glomerulonephritis
urine output 400ml or more in pxs with acute
or chronic azotemia

RENAL MANIFESTATIONS
CHARACTERISTICS OF IMPAIRED TUBULAR FUNCTION
Urinary sodium
>20 mmol
concentration
Usually is 40 mmol/L
Urine-to-plasma (U/P) ratio
<2
for urea
Urine-to-plasma (U/P) ratio
<20
for creatinine
Urine osmolality
<350 mmol/kg of water
Ratio of blood urea nitrogen
Not elevated
(BUN) to serum creatinine

PROTEINURIA
Normal adults may excrete up to 150 mg/d protein.
Of this, only 5 to 15 mg is albumin (<30 mg/d Harrisons 18th Ed.)
tested in pxs suspected of glomerulopathies
Massive proteinuria
Protein excretion >3.5 g/24 hrs
Nephrotic syndrome

SINGLE
NEPHRON
GFR (SNGFR)
Increased

REDUCED NEPHRON NUMBER

CLINICAL STATES

One kidney is removed, due to:

1. Surgical loss of renal substance,
secondary to:
Trauma
Neoplasm
Stone
2. Destruction of kidneys by:
Bacterial infection
Tuberculosis
Polycystic & medullary cystic renal
diseases
3. Chronic tubulointerstitial
nephropathies
What is expected:
Renal function is INCREASED
o The remaining kidney will compensate for
the loss of the other and will work doubletime
o May prone to develop injury
o Give precautionary measures and
appropriate diet.
o Try to diminish workload

Normal

SNGFR does not appear to increase despite a

reduction of nephron number in diseases where
the glomerulus is the primary site of damage,

TRANSCRIBED BY: LUKE, LEIA, HAN, CHEWBACCA

Combination of the following:

o Massive proteinuria
o Hypoalbuminemia
o Edema
o Hyperlipidemia
magnitude of proteinuria and the protein composition depend on the
mechanism of renal injury
charge and size selectivity normally prevent virtually all plasma
albumin, globulins, and other HMW proteins from crossing the
glomerular wall if barrier is disrupted plasma proteins may leak
(Glomerular proteinuria)
SMW proteins (<20 kDa) are freely filtered but are readily absorbed
by the proximal tubule
A. TUBULAR PROTEINURIA
Due to inability of the tubules to reabsorb the small molecular
weight proteins.
B. GLOMERULAR PROTEINURIA
Due to glomerular disease and abnormal permeability of the
glomerular capillaries to protein (usually with large molecular
weight proteins but no albumin)
HEMATURIA
Blood in the urine
2-5 RBCs per high-power field (HPF) and can be detected by dipstick
Think of 2 possible sources:
1. glomerular source: glomerulopathies
2. not glomerular (outside the kidneys)

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Renal Symptoms
Nov. 4, 2013

In glomerular hematuria:
RBC exposed to urine
Hypo-osmotic urine
Decreased osmolarity of the urine
Causes the RBCs to shrink: Dysmorphic RBC
Count the no. of RBC and the dysmormphic RBC
More than 85%:

Possible Glomerular Hematuria

Less than 50%:

Possible tubular hematuria or hematuria outside

kidneys (infection, stones, injury etc.)
From 2B 2016 trans:
female ask menstrual cycle
single urinalysis with hematuria is common and can result from:
o menstruation
o viral illness
o allergy
o exercise
o mild trauma
Gross hematuria
o with blood clots
o usually not an intrinsic renal process
o suggest a postrenal source
Persistent urinalysis
o >3 RBCs/HPF on 3 urinalyses, or gross hematuria
o associated with significant renal or urologic lesions in 9.1% of
cases
Isolated microscopic hematuria
o can be manifested by glomerular diseases

Syndromes associated with tubule dysfunction

Seen in renal tubular acidosis
o May have problems with PROXIMAL TUBULES:
Distal tubule will try to compensate and is unable to
compensate and reabsorb all.
(+) diuresis
o May have problems with DISTAL TUBULES:
Normal functioning proximal tubule but the distal continues
to excrete excess urine volume.
o May cause:
Loss of Sodium
Inability to reabsorb nutrients, sugar, vitamins
Cannot maintain acid base balance: Metabolic Acidosis

PRIMARY POLYDIPSIA
cause: unknown
increase fluid intake
results from habit, psychiatric disorder, neurologic lesions or
medications
NOCTURIA
Occurs during:

Reduced renal osmotic concentration

High sodium excretion

Solute diuresis

Low bladder capacity.

More than twice
Possibility: may also have polyuria

Dysuria
Glomerulonephritis

Na and H2O retention HTN

periorbital edema (puffiness oround the eyes) during the

morning

proteinuria

hematuria with dysmorphic RBCs, RBC casts, proteinuria

>500 mg/dL (virtually diagnostic)
Total hematuria

Isolated Hematuria

occurs evenly throughout voiding

blood has had the opportunity to mix
fully with the bladder urine
bleeding occurs mainly at the beginning or
end of micturition
without significant proteinuria, cells, or
urinary casts
prostatic or urethral origin is more likely
no significant findings
common causes of isolated hematuria
o urinary tract stones
o benign and malignant neoplasms of
the urinary tract
o tuberculosis
o trauma
o prostatitis
o few primary renal diseases

Urgency

Enuresis

Incontinence

Hirsutism

Virilization

ABNORMALITIES OF URINE VOLUME

POLYURIA
a urine volume above 3 L/d
quantification of urine volume by 24h urine collection
results from 2 possible mechanisms:
o
excretion of non-absorbable solutes (glucose)
o
excretion of water (defect in ADH prod.
responsiveness)
o
distinguished by urine osmolality
<250 mosmol/L water diuresis
>300 mosmol/L solute diuresis

Urinary
frequency

OTHER RENAL MANIFESTATIONS

Pain or a burning sensation during urination
Voiding at frequent intervals
Due to a sense of bladder fullness because of
an irritable bladder that feels full even when
it is not
Exaggerated sense of needing to urinate
Due to an irritable or inflamed bladder
Involuntary passage of urine at night or during
sleep hence the synonym bed-wetting
Bed-wetting without gross urologic
abnormalities
Inability to retain urine in the bladder
Results from neurologic or mechanical
disorders of the system that controls normal
micturition

or

renal

Overflow Incontinence
The inability to control urination.
Unable to completely empty the bladder
leading to overflow, which leaks out
unexpectedly
Male-pattern hair growth
Affects approximately 10% of women of
reproductive age
FEMALES ONLY
State in which androgen levels are sufficiently
high
Cause the following signs and symptoms:
o Deepening of the voice
o Breast atrophy
o Increased muscle bulk
o Clitoromegaly
o Increased libido
Ominous sign that suggests the possibility of
an ovarian or adrenal neoplasm

CLINICAL MANIFESTATIONS OF GLOMERULAR DISEASE

Asymptomatic

Macroscopic Hematuria
Diabetes Insipidus
Central: lack ADH

idiopathic

2o to hypothalamic conditions (posthypophysectomy, trauma,

neoplasm, inflammatory, vascular, or infectious)
Nephrogenic: not receptive to the effect of hormones (receptors)
Solute Diuresis
eg. Mannitol
Natriuretic Syndromes

TRANSCRIBED BY: LUKE, LEIA, HAN, CHEWBACCA

Nephritic Syndrome

Chronic
Glomerulonephritis
(CGN)

Proteinuria 150mg-3g/d
Hematuria > 2RBCs/HPF in spun
urine
Brown or red painless hematuria
Usually coincides with intercurrent
infection
Asymptomatic
Hematuria or proteinuria in between
attacks
Oliguria
Proteinuria usually <3g/d
Edema
HPN
Abrupt onset, usually self-limiting
HPN
Renal Insufficiency
Proteinuria > 3g/d
Small kidneys

Page 3 of 6

Renal Symptoms
Nov. 4, 2013

Rapidly Progressive
Glomerulonephritis
(RPGN)

Nephrotic Syndrome

Renal failure over days or weeks

Proteinuria usually <3g/d
RBC casts
BP often normal
Vasculitic features
Proteinuria >3.5g/d
Increased cholesterol
Decreased albumin
Lipiduria

DIFFERENCE BETWEEN NEPHROTIC AND NEPHRITIC

Features
Nephrotic
Nephritic
Onset
Insidious
Abrupt
Edema
++++
++
BP
Normal
Raised
JVP
Normal or low
Raised
Proteinuria
++++
++
Hematuria
May or may not occur
+++
RBC Casts
Absent
Present
Albumin
Low
Normal / slightly
decreased

Due to phosphate
precipitation

Urine pH

Urine
Protein

and lymphatics

CHEMICAL CHARACTERISTICS
Normal Values
Comments
4.5-8 (5-6)
pH
Possible Conditions
5
Uric acid stones
7
Vegetarian diet
Systemic acidosis
8
(renal-tubular
acidosis)
7-8
Struvite stones
Negative (<150 Mostly detects albumin
mg/ 24 hrs)
Possible
pH
Conditions
Trace
1-10mg/dl
+1
15-30mg/dl
+2
40-100mg/dl
+3
150-350mg/dl
+4
> 500mg/dl

MICROALBUMINURIA
edema in nephrotic syndrome is d/t massive proteinuria

TUBULOINTERSTITIAL DISEASES
Characterized by inflammatory scarring changes
Primarily involves tubules and interstitium
Relative sparing of the glomerulus and vasculature
CLINICAL PRESENTATION
As compared to glomerular causes of kidney diseases, patients with
tubular kidney disease progress in a slow progressive manner:

Slower rate of loss of renal function

Less severe systemic hypertension
No edema despite severe degree of renal insufficiency
Impaired concentrating capacity
(nocturia, polyuria)
Glycosuria w/o hyperglycemia
Low grade proteinuria
Electrolyte imbalance

1.
2.
3.
4.
5.
6.
7.
8.

COMMON CAUSES
Drug induced interstitial nephritis
(NSAIDs, rifampicin, lithium)
Infectious ( viral, bacterial , parasitic)
Malignancy (multiple myeloma, lymphoma)
Transplant rejection
Reflux Nephropathy
Obstructive Nephropathy
Metabolic (gout)
Radiation

CLINICAL ASSESSMENT OF RENAL FUNCTION

Urinalysis
Serum creatinine
Creatinine Clearance
Ultrasound
Radiologic Exam
Electrolytes
CBC

URINALYSIS
In contrast to GFR, urinalysis tells little about the severity of renal
disease but may point to a specific diagnosis.
A key feature of the assessment of any patient with renal disease
1. Physical Properties
2. Chemical Properties
3. Microscopy

Color
Specific
Gravity

Turbidity

PHYSICAL CHARACTERISTICS
Normal Values
Clinical Values
Yellow
May point to drug ingestion
(rifampicin)
1.003 - 1.030
1.000-1.005 in diabetes
insipidus
>1.030 due to contrast
dyes, glucose, mannitol
No clinical
Chyluria (milky white) due
significance
to fistula between bladder

TRANSCRIBED BY: LUKE, LEIA, HAN, CHEWBACCA

Urine albumin concentration >30ug/min or 30mg/day

Most of the urinary proteins are low molecular weight proteins like
Tamm-Horsfall proteins.

ALBUMIN CREATININE RATIO

More accurate method.

Example: ratio of <0.2mg protein/mg creatinine (< 22mg

protein/mmol creatinine) equates to urine protein of <
0.2g/24h
NORMAL URINE MICROSCOPY

CELLS AND CASTS

Leucocytes
Erythrocytes
Tubular cells
Hyaline casts
Granular casts
low power field (LPF)
high power field (HPF)

Eosinophils
Epithelial
Cells

LIGHT MICROSCOPY PER FIELD

1-4 /HPF
1-2 /HPF
1/10 HPF
1/ LPF
1/ LPF

OTHER CELLS
Seen in allergic nephritis
Squamous
Least significant
Transitional
From pelvis to urethral lining
Renal tubular Most significant, consider
acute tubular necrosis

Hyaline Cast
Non-pathologic, seen commonly in
dehydrated patients (small urine
volume/diuretics)
Made up of Tamm-Horsfall protein
Broad Waxy Cast
Made up of both the granular and
hyaline casts and is due to urine
flow stasis in the collecting ducts or
distended renal tubules.
Extreme stasis of flow
May be seen in renal failure
Fatty Cast
Seen in patients with nephrotic
syndrome

WBC Cast
Made up of PMNs, indicative of
Pyelonephritis and acute interstitial
nephritis

Page 4 of 6

Renal Symptoms
Nov. 4, 2013

RBC Cast
Seen in glomerulonephritis and
sometimes in strenuous exercises

Dysmorphic RBC
Due to longer contact with urine
Dysmorphic
RBCs (%)
>85
<50
50 85

Possible Origin
of Disease
Glomerular
Tubular
Urinary tract

Granular Cast
Fine Granular Casts are derived
from disintegration of cellular casts,
from tubule cell lysosomes, protein
aggregates.
Can be seen in GN
(glomerulonephritis), PN
(pyelonephritis) and strenuous
exercise
With surrounding amorphous urates

CREATININE CLEARANCE
Creatinine Clearance
= (Urinary creatinine (mg/ml) x Urinary Volume) x 100 / Serum
creatinine (24 hr urine collection)
Widely used method to estimate GFR
Quick estimation of creatinine clearance from plasma (CockcroftGault) formula

COCKROFT GAULT FORMULA

Coarse Granular Cast

(140 Age ) X Wt in kg
72 X Cr in mgs/dl
multiply result by 0.85 for female

SERUM CREATININE
Mainly derived from metabolism of creatine/creatine phosphokinase
from skeletal muscle cells
Produced at almost constant rate
Steady state concentration dependent on renal excretion w/c mainly
reflects of GFR

RELATIONSHIP BETWEEN PLASMA CREATININE AND GFR

A quick look at the graph tells us of the inverse relationship between
plasma creatinine (Pcr) and
the GFR. Considering this
graph, we should remember 3
important things:

Normal Values for Creatinine Clearance Rate

Males
120 25ml/min (about 175L/day)
Females
95 20ml/min (about 135L/day)
*Normal decline rate of 1ml/min/yr after 40y/o
ULTRASOUND
Normal kidney size is between 9 to 10 cm
Renal cortices about 1 cm in thickness and smooth in contour
Ultrasound has become a very popular examination of the urinary
tract because of its simplicity, low cost, non-invasiveness & low risk

(1) This curve is only valid in

the steady state when
the Pcr is stable.
(2) Note the shape of the
curve, in pts. With
normal renal function,
an increase in the level
of
creatinine
from
1mg/dl
to
1.5mg/dl
represents a marked fall
in the GFR (from 120 to
80 ml/min). Whereas in
pts. with advanced renal
failure, a marked increase in level of creatinine, from 6mg/dl to 12
mg/dl only translates into minimal reduction in GFR from
20ml/min to 10 ml/min.
(3) Their relationship is dependent upon rate of creatinine production.
Therefore it is not the absolute value of plasma creatinine that we
gauge and monitor in renal failure but the change from one value
to another (serial monitoring).

USES OF ULTRASOUND: DETECTION

1.
2.
3.
4.

Renal mass
Renal failure
Stone disease or obstruction
Perirenal
and
pararenal
(urinoma, hematoma, abscess)
5. Transplant dysfunction
6. Cystic diseases
7. Prostate disease

Plain Film of
Abdomen
Contrast Films

TRANSCRIBED BY: LUKE, LEIA, HAN, CHEWBACCA

spaces

disease

RADIOLOGY
Used to assess bone, soft tissue changes,
calcifications, renal location
Series of films taken at varying time after
contrast administration

Page 5 of 6

Renal Symptoms
Nov. 4, 2013

INTRAVENOUS UROGRAPHY
Fairly accurate diagnostic procedure when properly done

At 30 min
At 5 10 min

Maximum visualization of the renal parenchyma

Collecting system, ureters, bladder

Normal IVP showing filling of

ureters w/ contrast dye from the
pelvis to the bladder.

Nocturia in venous insufficiency due to increased preload or

increased circulating blood volume
Dysuria there is burning sensation while urinating
Crescent formation

hallmark of
rapidly
progressive
glomerulonephritis (RPGN)
Reflux nephropathy there is development of recurrent UTI
especially in children; due to congenital diseases
Obstructive nephropathy recurrent UTI not related to STDs
Obstruction in the urethra, bladder extrarenal cause
Obstruction in the tubules intrarenal cause
Intrarenal obstruction usually due to gout leads to uric acid
nephropathy
Chemotherapy destroys a lot of cells will increase uric acid
excretion may also obstruct the tubules (intrarenal obstruction)
Pyuria consider glomerulopathies (proliferative)

Showed a delayed nephrogram

due to a stone in the left mid
ureter

RETROGRADE PYELOGRAPHY
Placement of catheter through urethra by cystoscopy advancing to
renal pelvis
Information on possible filling defects, obstructing lesion especially
length of obstruction and ureter distal to the obstruction

ANTEROGRADE PYELOGRAPHY
Contrast procedure via percutaneous renal puncture.

TAKE-HOME MESSAGES (2D 2016)

1. Pyuria or presence of pus cells in the urine does not always equate
to urinary tract infection.
2. After establishing working diagnosis, we should be able to estimate
the degree of renal dysfunction.
3. If the creatinine is 2mg/dl, it is best to refer the patient to a kidney
specialist.
4. If with significant proteinuria despite normal creatinine levels, best to
refer to a kidney specialist.
2C 2015 NOTES:
25% of cardiac output goes to the kidneys
Change in sleeping pattern earliest manifestation of uremia
Anorexia, nausea and vomiting more noticeable manifestations of
uremia
Uremia absolute indication for dialysis
GFR is dependent on blood flow
Prerenal azotemia tubules are still intact i.e., can still concentrate
sodium; maintain electrolyte and acid base balance; but GFR is
decreased
Postrenal azotemia due to acute obstruction lowers single
nephron GFR (SNGFR)
GI loss most common cause of hypovolemia
Prostate cancer most common cause of painless hematuria
Acidosis + Urine pH is basic tubule dysfunction
Obligate water loss 500 cc/day
Increase urine sodium of >20-40mmol/liter despite hypovolemia
acute tubular necrosis (ATN) or acute renal failure (ARF)
Prerenal azotemia fluids may still be excreted
Renal failure fluids may not be excreted anymore
Cause of bilateral kidney obstruction benign prostatic hyperplasia
(BPH), pregnancy
Oliguria = <400cc/day urine output
Anuria = <40 cc/day urine output
Polyuria = >3L/day urine output
Proteinuria of >3.5g/24hrs or 1.7m 2/body surface area massive
proteinuria may lead to nephrotic syndrome
Tamm-Horsfall proteins filtered proteins
Bence-Jones proteins multiple myeloma
Glomerular proteins high molecular weight proteins
Hematuria consider prostate or urethral origin
Isolated hematuria no proteins, casts, cells in the urine; only
hematuria is present
Central diabetes insipdius decreased ADH
Nephrogenic diabetes insipidus increased ADH but the kidneys
are not responsive
Mannitol causes solute diuresis
Natriuretic syndromes there is development of renal-tubular
acidosis (RTA)
Primary polydipsia (idiopathic) patient drinks a lot of water
polyuria, nocturia

TRANSCRIBED BY: LUKE, LEIA, HAN, CHEWBACCA

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