TOP 10 NEPHRO SLIDES

IN BOARD EXAMS

BOARD EXAM SLIDES

WHAT IS THIS ?

WHAT IS THIS ?

WHAT IS THIS ?

WHAT IS THIS ?

WHAT IS THIS ?

WHAT IS THIS ?

WHAT IS THIS ?

COMMONEST NEPHRO CASES IN

BOARD EXAM TRICKS AND CLUES

MOST OF THE CASES CONTAIN ONE SINGLE

OUTSTANDING CLUE THAT CAN GIVE YOU
THE DIAGNOSIS --LOOK FOR THAT CLUE

THIS IS THE M-KASAP TYPE OF QUESTIONS

GLOMERULONEPHRITIS EXAM
TRICKS AND CLUES

A.RBC CASTS:
1. MPGN
2.IGA
3.POST STREP GN
4.SLE NEPRITIS
5.RPGN AS ANCE NEPHRITIDES

CONTINUES CLUES

A PATIENT WITH GLOMERULAR PROTIENUREA

AND INCREASED LIVER ENZYMES IS MPGN
DUE TO HEP C

A PATIENT OBESE WITH PROTIENUREA IS

FSGS

CONTINUE

A PATIENT WITH HEROIN ABUSE AND

PROTIENUREA IS FSGS

A PATIENT WITH PROTIENUREA AND RENAL

IMPAIRMENT AND FEW + DIPSTICK WITH
LARGR TOTAL 24 HRS PROTIENUREA ID M
MYELOMA

CONTINUES

A PATIENT ON NSAID AND PROTIENUREA IS

MMD
A PATIENT WITH CANCER AND NEPHROTIC
PROTIENUREA IS MGN EXCEPT IF HE HAS
HODJKINS LYPHOMA IT IS MIN CHANGE
DISEASE

CORRECT ANSWER IS A

CHOLESTEROL EMBOLISATATION
ONE OF THE MOST AND TOP QUESTIONS IN
ARAB-SAUDI-AMERICAN BOARD EXAMS

SIMPLY EXAMINERS THEY LOVE IT !!!

I TOLD U LOOK FOR THE CLUE!!

WHERE IS THE CLUE HERE ?

THE CLUE IS THE TIME OF INCREASE IN CR

WHICH IS AFTER 48 HRS
CONTRAST GIVE U INCREASE CR WITHIN
FIRST 24 HRS OF THE ANGIO BUT CE THE
RISE IS AFTER 48 HRS
OTHER CLUES LOW COMPLEMENTS,AND
HIGH ESR

CE-CASE

ESINOPHILLIA
DIGITAL INFARCTS
LIVEDO RETICULARIS
RETINAL EMBOLI AND HEMORRHAGES
RISK INCREASED BY HEPARINE
AS CTD
PROGNOSIS GRAVE ( NO SINGLE CASE HAS BEEN
RECOVERED

Cr timing

Cr increase in contrast within first 24 hrs

Cr increase in embolisation after 24-72 hrs

Cr increase in gentamycine after 7-10 days

All the follwing are true of

preclampcia EXCEPT :

A. high uric acid

B. high Cr
C. no urine RBC casts
D. high urine calcium
E. high urine protien

36 yrs female known case of SLE

want to become pregnant, what
would u advice her ?

A. the single most important is Cr level at the

time of conception
B.the single most important is disease activity
level at conception
C.the single most imprtant is protienurea
D.A AND B
E.B AND C

25 OLD MALE COCCAINE ABUSER

PRESENTED TO ER WITH :

VOMITING,HYPERTENTION,AND FEVER WITH

DECREASE URINE OUTPUT
O/E BP 170 / 98 T 38
CVS S1,S2 NORMAL WITH ESM
LUNGS CLEAR,ABD NO ORGANOMEGALY
HX OF CHANGE OF URINE COLOUR

LABS

CBC WBC 7,PLAT 230,Hb 10.6

LFT NORMAL
Cr 600 AND ONE MONTH AGO WAS 78
Na 137, K 6.8,Ca 1.2,Ph 1.9
Uric Acid 600
UA POSITIVE FOR BLOOD +++ ON
DIPSTICK,PROT +,RBC 1-5

THE MOST LIKELY DX:

A. RHABDOMYOLYSIS
B. SBE
C.TUMOR LYSIS SYNDROME
D.POST INF GN
E.POLYARTERITIS NODOSA

RHABDOMYOLYSIS-THINGS IN
EXAM TO REMEMBER

THE COMMONEST CAUSE IS TRUMA-SOLDIER

SYNDROME
THE COMMONEST DRUG IS COCCAINE
OTHER DRUGS HMG-COENZ-RED-INHIBITORS
AS STATINS
THE SINGLE MOST IMPORTANT STEP IN
MANAG IS IVF AND IVF AND IVF

COMMON MCQ IN EXAMS-GN

54 YRS MALE PRESENTED WITH

WEAKNESS,DIAZINESS, FOR 4 MONTHS
CBS HB 8GM,WBC 5,PLAT 230
LFT Na 137,K 6,Ca 2.6,
U/A DIPSTICK PROTIEN +,BLOOD
MICROSCOPY NO RBC CASTS
TOTAL 24 HRS PROTIEN 8 GM

RENAL BX;

THE MOST LIKELY DX IS ;

A.AMYLOIDOSIS
B.MYELOMA KIDNEY
C.MEMRANOUS GN
D.FSGS
E.MINIMAL CHANGE DISEASE

MYELOMA KIDNEY-EXAM
FAVOURITE

THE MOST IMPORTANT CLUE IN EXAM IS

DIPSTICK URINE NEGATIVE FOR PROTIEN OR
MILD + POSITIVE BUT THE 24 HRS URINE
COLLECTION FOR PROTIEN IS MORE THAN 3
GM. WHY ?
LARGE KIDNEY. WHAT OTHER CAUSES OF
LARGE KIDNEY ????

TWO TYPES OF MYELOMA KIDNEY

A. TUBULAR WITH LIGHT CHAIN DEPOSITION

AND GIVE U FRACTURED CAST DIAGNOSTIC
OF MM.THIS TYPE HAS GOOD PROGNOSIS
B.LDD-CHARACTERISED BY NODULAR
SCELEROSIS AND POOR PROGNOSIS

MEMBRANOUS GN-EXAM POINTS

THE COMMONEST CAUSE OF RENAL VIEN

THROMBOSIS
THE COMMONEST CAUSE OF NEPHROTIC
SYNDROME IN ADULTS
COMPLEMENTS NORMAL,NO RBC CASTS
ASSOCCIATED WITH MALIGNANCY COLON

MGN

IDIOPATHIC
SECONDARY TO DRUGS ( ACE,GOLD,PENCILLAMINE )
INFECTIONS(MALARIA,HEP B)
TREATMENT( ACE,PONTICELLI
PROTOCOL=CHLORAMPUCIL ALTERNATING WITH
STEROIDS OR IMMURAN
RESISTANT USE CYCLOSPORINE

PROGNOSIS-THE 25 % DISEASE

25 % COMPLETE RECOVERY
25 % PARTIAL RECOVERY
25 % ESRD
25 % RELAPSE ON AND OFF

FSGS-EXAM QUESTIONS

THE COMMONEST QUESTIONS IS CAUSES

OR A CASE WHICH TELL U THE CAUSE
OBESE PATIENT WITH PROTIENUREA IS FSGS
A PATIENT WITH HIV THE COOMNEST RENAL
BX FINDING IS COOLAPSING FSGS
A PATIENT ON HEROINE OR DRUG ABUSER IS
FSGS OR INF-@

FSGS

A PATIENT WITH SINGLE KIDNEY AND

PROTIENUREA IS FSGS
A PATIENT WITH REFLUX HAS FSGS
STEROIDS CAN INDUSE REMISSION IN 40 %
OF CASES
IT IS THE HIGHEST AND FASTEST
RECURRENCE OF RENAL TX WITH MPGN

HIV NEPHROPATHY

POINTS TO REMEMBER IN EXAMS:

1.LARGE KIDNEY
2.CYSTIC TUBULAR DILATATION
3.ENDTHELIAL CYTOPLASMIC
RETICLOTUBULAR STRUCTURES ON EM
4.COLLAPSING FSGS IS THE COMMONEST
VARIETY

MCD-EXAM QUESTIOS

NSAID IS THE ONLY DRUG KNOWN TO CAUSE

MCD WITH INF-@
ALL MALIGNANCY ASSOCIATED WITH
MEMBRANOUS GN EXCEPT ONE MLIGNANCY
ASSOCIATED WITH MCD DO U KNOW WHAT IT
IS ????????????
Hodgkins lymphoma.

MCD-EXAM POINTS
IN A PATIENT WITH MCD WHO IS NOT RESPONDING TO
ADEQUATE COURSE OF STEROIDS THE MOST LIKELY
CAUSE IS FSGS SO DO RENAL BX
THE MOST IMPORTANT POINTS ABOUT MCD IS THIS
IN CHILDREN A COURSE OF 8 WEEKS STEROIDS IS
ADEQUATE TO INDUSE REMISSION

BUT IN ADULTS THE STORY IS

DIFFERENT

IN ADULTS DO NOT LABEL THE PATIENT AS

STEROIDS RESISTANT UNLESS U GIVE 12
WEEKS OF STEROIDS
REMEMBER AT LEAST 12 WEEKS
DO U KNOW THE DIFFERENCE BETWEEN
STEROIDS DEPENDENT AND STEROIDS
RESISTANT AND STEROIDS RELAPSER

MPGN-EXAM POINTS

THE HIGHEST RECURRENCE OF DISEASE IN

TX ( 80 % )
THE COMMONEST CAUSE OF MPGN IN THE
WORLD NOW IS Hepatitis C
CRYOGLOBULINEMIA IS IMPORTANT CAUSE

FREQUENT AND COMMON BOARD

EXAM QUESTION IS THIS ONE

54 YRS MALE PRESENTED WITH HEAVY

PROTIENUREA OF 7GM
HIS LFT IS ABNORMALA
THE RENAL BIOBSY WILL
SHOW.

RPGN-THE MOST FREQUNT

QUESTION COMES IN EXAMS

IT IS A MEDICAL EMERGENCY
IN FACT IT IS THE ONLY GN THAT IS
EMERGENCY
IT CAN KILL THE KIDNEY IN 72 HRS IF U DID
NOT ACT
U START RX EVEN BEFORE THE BX RESULT

CAUSES;

WEGNERS
PAN
CHURG-STRAUSS
ANTI-GBM

Case presentation

58 yrs male working as a business man

Started to have muscle weakness,fever,wight
loss,and bloody urine ,hemoptysis,and new
hypertention for the last 3 months .
BP 210/ 12O
His Cr 6 months ago was 120 ,now 440
ESR 89

P-ANCA

WEGNERS
MICROSCOPIC POLYANGIOPATHY
CHURG-STRAUSS
IDIOPATHIC RPGN IN THE ELDERLY

REVERSAL OF RENAL FUNCTION IN

ANTI-GBM DISEASE(GODPASTUER)

IF Cr LESS THAN 550

IF PATIENT NOT YET STARTED ON DIALYSIS
IF PLASMAPHRESIS STARTED EARLY

BEST RX FOR GODPASTURE

PLASMAPHRESIS

PULSE IV STEROIDS

BEST RX FOR WEGNERS

PULSE IV STEROIDS

CYCLOPHOS

PLASMAPHRESIS

C-ANCA-ONLY WEGNERS

THE MOST IMPORTANT SLIDE IN

GLOMERULONEPHRITIS

ANY CASE IN THE EXAM MENTION UA

CONTAIN RBC-CAST

THERE ARE ONLY 5 DDX IN MEDICINE

DO U KNOW WHAT ARE THEY ??????? ??

CAUSES OF RBC-CAST THIS IS

CALLED ACTIVE URINE SEDIMENT

1. MPGN
2.IGA NEPHROPATHY
3.POST-INFECTIOUS GN AS POSTSTREPTOCOCCAL GN
4.SLE
5.RPGN

WHAT IS THE SINGLE

MOST IMPORTANT TEST
TO DIFFRENTIATE
BETWEEN
PRERENAL
AND POSTRENAL
AZOTEMIA ( ATN ) ??

IT IS FENA

PROXIMAL RTA
MA

WITH NORM AG
URINE PH < 6 ACIDIFY THE URINE
DISTAL RTA ALWAYS URINE PH >6
DISTAL RTA GIVE LOW HCO3

CONTINUE
DISTAL

RTA SEVERE MUSCLE

WEAKNESS AND VERY LOW HCO3
PROX RTA GLYCOSURIA
AMINOCIDUREA

RTA TYPE 4
HYPORENEMIC
HYPOALDO
HYPERKALEMIC
HYPERCHLREMIC
MA
DM

CEREBRAL SALT WATING

CSW
HYPONATREMIA
HIGH

URINE OSMOL >600 AND

HIGH U NA >100
HYPOVOLEMIA WITH
ORTHOSTATIC DROP BP
SIADH NO VOLUME DEPL AND
URIC ACID IS VERY LOW

Isopropyl alchol

NO MA

SERUM AND URINE KETONES++

HIGH OSMOLAL GAP

Q 8 MKSAP 15

TOLUENE
MA
SEVERE HYPOKALEMIA
HYPOPHOSPHATEMIA
CPK ENZYME HIGH
RHABDOMYOLYSIS

22 yrs male found comatose and his

friends mention that he had
problems with his wife and
attempted suicide and his labs;
Na 140,k 5,cl 95,CO2 10,GLUCOSE
7,PLASMA OSMOL 325,BUN 13

PH 7.1,PCO2 24,PO2 85

WHAT ACID BASE DISTURBANCE ?

IS IT SIMPLE OR MIXED ?
WHAT IS THE DX ?

Expected PCO2 = 1.5 X HCO3 + 8 ( +

OR 2 )

MA WITH HIGH AG
EXP PCO2 IS 21 25
MA POISONING

5-DAYS LATER HIS ABG :

PH 7.2
HCO3 16
PCO2 45

WHAT ACID BASE IS THIS ?

EXP PCO2=1.5 X 16 + 8=32

BUT PCO2 IS 45 SO THIS IS MIXED MA + RESP

ACIDOSIS

Where do u see it???

ASA LATE STAGE

SEPSIS

COPD + SEPSIS

NORMAL AG

IF AG NORMAL THINK OF RTA AND

DIARRHEA THEN LOOK AT THE UA GAP

UA AG= (NA + K )- CL IF THE CHARGE IS
NEGATIVE IT IS DIARRHEA AND IF + IT IS RTA

If urinary K more than 10 there are

only 8 causes in medicine

Vomiting ( the commonest )

Diuretics
Mineral corticoid Excess( conn syndrome )
Licorice
Cushing
RTA
Barters / Gitelman
Mg low ( the forgotton one )

Case presentation

34 yrs old female presents with severe

hypertensions BP 200 / 120 .EXAM NEGATIVE
Apart from LL OEDEMA
Serum K 2.5 AND URINE K 60
Resting PRA 60,Aldosterone 100 ng/dl
Renal Angiogram shows normal renal arteries
and vascular blush

Case presentation

25 yrs old male with new onset High BP

BP 180 / 11O,P90,Hypertensive retinopathy,S4
gallop
UA + protein
Labs Na 140,K2.4,Cl 97,HCO3 30,PH 7.44
Cr 80,PRA 0.1 ng/ml/hr ( low ),plasma
Aldosterone 4 ng/dl (low)
24 hrs urine Na 200 mEq,K 40mEq

28 yrs male DX as HIV developed

PCP and was started on iv septra?

Serum Na 135,CL 90,K 6

PH 7.36,Cr 70,
What is the most likely cause of hyperkalemia ?

35 yrs male post renal TX on CS

A,Pred and cellcept?

Serum K 6,Na 138,CL 114,HCO3 15

Cr 80
What is the most likely DX and cause of
hyperkaemia ?

30 yrs male admitted with

pulmonary embolism and started on
anticoagulant?

Serum Na 128,K 6,Cr 67

HCO 24,Mg 1,Ca 2.8
What is the most likely cause of hyperkalemia?

TTKG
TTKG= (KU) X BLOOD OSMOL
-----------------------------(K BLOOD) X U OSMOL

TTKG

UK XPLASMA OSMOL=14 X 285 = 3990

PLASMA K X URINE OSMOL= 6.4X 351=2246

TTKG= 3990 / 2246 = 1.7

THIS IS MINERALOCORTICOID INSUFF

25 yrs female presented with

muscular weakness?

K 2.5, HCO3 32,PH 7.48,Mg normal

Urinary K 40, urine CL 150
Bp is normal
What is ur DDX and most likely DX ?

If urinary K more than 10 there are

only 8 causes in medicine

Vomiting ( the commonest )

Diuretics
Mineral corticoid Excess( conn syndrome )
Licorice
Cushing
RTA
Barters / Gitelman
Mg low ( the forgotton one )

DDX OF HIGH URINE K WITH

HYPOKALEMIA

Vomiting? NO Because urine CL is high .in

vomiting and any volume depletion the first
electrolyte to be down in urine is CL BECAUSE
Na will be normal initially and later will be low
,but CL WILL BE LOW FROM THE START

IS IT RTA?

RTA ? No ? Because there is no metabolic

acidosis HER PH IS ALKALOTIC

IS IT CONN OR CUSHING?

NO BECAUSE BP IS NORMAL AND NO SIGN OF

CUSHING CLINICALLY

SO HER DDX SHOULD BE ONE OF

THESE TWO:

DIURETIC ABUSE
BARTTAR / GITELMAN

GITELMANS AND BARTTARS

Gitelman syndrome is a rare inherited defect in

the distal convoluted

Bartter syndrome, which is a rare inherited

defect in the thick ascending limb of the
loop of Henle.

Gitelman's syndrome

identical to those of patients

who are on thiazide diuretics

Clinical symptoms for this disease are

hypochloremic metabolic alkalosis,
hypokalemia, and hypocalciuria.
Hypomagnesemia is present in many but not all
cases.

BARTTERS
Evidence

for a tubular defect in the loop of

Henle
an inherited defect in the renal tubules that causes
low potassium levels, low chloride levels, which in
turn causes metabolic alkalosis. Bartter Syndrome,
is not a single disorder but rather a set of closely
related disorders.

Bartter and Related

Syndromes, the Puzzle is
Almost Solved

can be divided into

three different genetic
and clinical entities

Bartter syndromes are defined as a family of

inherited recessive autosomal tubulopathies.
They are characterized by hypochloremia,
hypokalemia, metabolic alkalosis associated
with potassium renal leakage and normal
blood pressure despite increased plasma
renin activity.

hypercalciuria and nephrocalcinosis

This lady should have one of the

following:
Diuretics

abuse
Barttar/gitelman syndrome
Why ???

The Four golden keys to make DX of

Hypokalemia :

URINE K

BP

ACID-BASE STATUS

Mg level

ABDOMINAL CT WITH IODINATED

CONTRAST
IT IS THE PROCEDURE OF CHOICE IN
CKD PATIENTS ON DIALYSIS FOR
DIAGNOSING MALIGNANCY CHANGE
IN CYSTS OF KIDNEY
REMEMBER MRI WITH GADOLINIUM
CONTRAST

CONTINUE
CAN CAUSE NSF CHARACTERIZED BY
EDEMA AND THICKENED SKINS OF
HAND AND FEET
HIGHEST RISK IS WITH GFR
<40ML/MIN
MKSAP Q 12 NEPH EDIT 15

A DYNAMIC BONE DISEASEMKSAP Q19ED15

COMMONEST BONE DISEASE IN PAT ON

PERITON DIALYSIS
COMMONEST IN DM
BONY PAIN ,OSTEOPENIA,PTH <100 AND
NORMAL ALK PHOSPH

B2-MICROGLOBULIN

AMYLOID
X-RAY LARGE CYSTS DILATED AT LONG
BONES ENDS
OSTITIS FIBROSA CYSTICA

In patients with recurrent calcium

oxalate stones and hyperoxaluria,
increased dietary calcium intake and
avoidance of oxalate-rich foods such
as rhubarb, peanuts, spinach, beets,
and chocolate are recommended to
.decrease the risk of stone formation

Key Point
In patients with chronic kidney disease,
iron deficiency anemia should be
corrected before initiation of an
. erythropoiesis-stimulating agent

Key Point
In patients with symptomatic, acute
hyponatremia, rapid normalization of the
extracellular fluid osmolality with
. hypertonic saline is indicated

Key Point
Adherence to a high-calcium diet
(generally defined as 1 to 4 g/d of
calcium) has been shown to decrease the
risk of incident and recurrent calcium
. oxalate stone formation

The cathartic agent sodium

phosphate may cause acute
phosphate nephropathy resulting in
acute kidney injury and
hyperphosphatemia out of proportion
to the degree of kidney failure

Key Point
Obstructive nephropathy must always be
included in the differential diagnosis of a
patient with acute kidney injury to ensure
prompt diagnosis and reversal of kidney
. injury

Key Point
The target blood pressure in patients with
type 2 diabetes mellitus and nondiabetic
chronic kidney disease in the absence of
.proteinuria is less than 130/80 mm Hg

Ethylene glycol poisoning is

associated with an anion gap
metabolic acidosis, an increased
osmolal gap, kidney injury, and
calcium oxalate crystals in the
.urine

Key Point
Angiotensin receptor antagonists and
angiotensin-converting enzyme
inhibitors are contraindicated during
.pregnancy

Key Point
In the hospital setting, patients with chronic alcoholism
may have normal serum phosphorus levels on admission
to the hospital but often develop severe
hypophosphatemia over the first 12 to 24 hours

Severe hypophosphatemia often develops over the first 12

to 24 hours after admission, usually because of
intravenous glucose administration. This agent helps to
release insulin and rapidly reverses alcoholic ketoacidosis,
which causes phosphate to shift into cells.

The sudden development of

hypophosphatemia may cause
confusion, rhabdomyolysis,
hemolytic anemia, and severe
muscle weakness that can
lead to respiratory failure.

Key Point
In patients with chronic kidney
disease who have persistent
hypertension and proteinuria, a
diuretic should be added if an
angiotensin-converting enzyme
inhibitor or angiotensin receptor
blocker and restriction of dietary
.sodium are not helpful

Key Point
The most common cause of HIVassociated nephropathy is collapsing
focal segmental glomerulosclerosis,
which is characterized by massive
. proteinuria

Key Point
Corticosteroid therapy is the initial
treatment of choice in patients with
minimal change disease, which is
characterized by the sudden development
of an elevated urine protein-creatinine
. ratio that may exceed 9 mg/mg

Key Point
Lithium-induced nephrotoxicity may
manifest as nephrogenic diabetes
.insipidus and typically progresses slowly

Key Point
Isopropyl alcohol poisoning is
characterized by an increased osmolal
gap in the setting of positive serum and
urine ketones and does not cause
.metabolic acidosis

Key Point
Ambulatory blood pressure monitoring
is the gold standard for diagnosing
. white coat hypertension

Key Point
Proximal (type 2) renal tubular acidosis
secondary to multiple myeloma is
characterized by a normal anion gap
metabolic acidosis, hypokalemia, and an
. intact ability to lower the urine pH

Key Point
The diagnosis of polycystic kidney
disease can be confirmed by the presence
of at least two cysts in each kidney on
kidney ultrasonography in a patient with
a family history of this condition

Key Point
The most important risk factor for
intracranial aneurysm in patients with
autosomal-dominant polycystic kidney
disease is a family member with an
intracranial aneurysm

Key Point
Chronic kidney disease is the most
likely diagnosis in patients with
elevated serum creatinine levels and
. proteinuria early in pregnancy

Key Point
Immune complexmediated glomerular
nephritis is characterized by
hypocomplementemia and dysmorphic
erythrocytes and erythrocyte casts
. seen on urinalysis

Key Point
Dietary protein restriction and an
angiotensin-converting enzyme inhibitor or
angiotensin receptor blocker can be tried
for 6 months in patients with membranous
nephropathy who have a urine proteincreatinine ratio of 4 to 8 mg/mg and normal
. kidney function

Key Point
Kidney biopsy is the study of choice in
adults when the nephrotic syndrome is
suspected and helps to differentiate
among the causes of this conditio

Key Point
Alkalinization of the urine with potassium
citrate therapy to obtain a urine pH above
6.0 decreases the risk of recurrent uric
. acid stones

Key Point
Cerebral salt wasting may affect patients
undergoing neurosurgery, particularly
those with subarachnoid hemorrhage,
and manifests as hyponatremia, increased
urine sodium excretion, concentrated
urine, and evidence of hypovolemia

Key Point
Manifestations of primary aldosteronism
include hypernatremia, hypokalemia,
mild metabolic alkalosis, suppressed
plasma renin activity, and stage 2
. hypertension

In addition to therapy to inhibit the

renin-angiotensin system,
immunosuppressive therapy is
indicated in patients with IgA
nephropathy at risk for progression to
kidney failure who do not yet have
. significant loss of kidney function

type 1 diabetes mellitus who have

abnormal findings on annual measurement
of the urine albumin excretion should
undergo repeat urinalyses twice within the
next 6 months; positive findings on two of
the three urine samples would confirm a
diagnosis of microalbuminuria (defined as
a urine albumin-creatinine ratio between
30 and 300 mg/g).

Key Point
Salicylate toxicity is a common cause
of mixed anion gap metabolic
. acidosis and respiratory alkalosis

Key Point
The accuracy of timed urine collection can be
assessed by comparing the total urine
creatinine excretion with the expected value
of creatinine excretion

the expected value of creatinine

excretion (20 to 25 mg/kg/24 h (20 to
25 mg/kg/d) in men, 15 to 20 mg/kg/24
h in women

Key Point
The gold standard for diagnosing
renovascular hypertension is intraarterial digital subtraction
. angiography

Key Point
In patients with nonglomerular
hematuria, kidney ultrasonography and
cystoscopy are indicated to exclude a
genitourinary tract malignancy in
individuals with risk factors for this
. condition

Key Point
Diagnosis of AL amyloidosis is
established by
Abdominal fat pad biopsy

Clinical trials suggest that medical

therapy rather than angioplasty or
revascularization can effectively manage
renovascular hypertension secondary to
atherosclerosis and may be the best
option for patients with well-controlled
blood pressure on medical therapy alone.
Referral to a nephrologist

Manage a patient with myeloma cast

nephropathy
Hemodialysis, plasmapheresis, and
chemotherapy

Methyldopa and labetalol are safe for

treatment of hypertension during
. pregnancy

Multiple myeloma may manifest

as hypercalcemia, anemia, kidney
insufficiency, and proximal (type
2) renal tubular acidosis

Key Point
Kidney manifestations of sarcoidosis
include interstitial nephritis with
granuloma formation,
hypercalciuria, nephrocalcinosis,
. and various glomerular diseases

Key Point
The treatment of choice for
. pheochromocytoma is surgical resection

Key Point
Prerenal disease is usually associated with
a fractional excretion of sodium of less than
1%, but this value is usually higher in
.patients with chronic kidney disease

Key Point
Nephrostomy tube placement is indicated to
manage urinary tract obstruction associated
with acute kidney injury when the obstruction
is not relieved with bladder catheter
. placement

Manage hypertension in a patient more

than 80 years of age.

Hydrochlorothiazide

Diagnose bone disease due to secondary

hyperparathyroidism in a patient with endstage kidney disease.
associated with elevated serum parathyroid
hormone and alkaline phosphatase levels,
hyperphosphatemia, and hypocalcemia.

Key Point
Acute tubular necrosis usually develops after
a sustained period of ischemia or exposure to
nephrotoxic agents such as cisplatin,
intravenous aminoglycosides, or radiocontrast
and is associated with muddy brown casts on
urinalysis

Key Point
Use of tacrolimus and another
cytochrome P450 3A4 inhibitor can
cause tacrolimus toxicity, which may
. lead to acute kidney dysfunction
Erythromycin

Key Point
Surgical resection is indicated for patients
. with Bosniak category III and IV kidney cysts
Complex cystic structures or mass lesions,
especially those greater than 4 cm, should
raise suspicion for malignancy

Bosniak category III cysts are

characterized by irregularly shaped walls
with septal calcification. These cysts
enhance after the administration of
iodinated contrast agents. Approximately
50% of Bosniak category III cysts are
malignant; therefore, surgical resection
is indicated for patients with these cysts.

Mineralocorticoid receptor antagonists

are particularly effective in treating
. resistant hypertension
Spironolactone

Diagnose polyarteritis nodosa as a cause

of kidney failure.
Angiography of the renal arteries

Key Point
Percutaneous nephrolithotomy is the
treatment of choice in patients with
. staghorn calculi
This intervention allows for direct
visualization of the kidney and verification of
stone removal via nephroscopy and is
associated with an estimated initial cure rate
of 80%.