TOP 10 NEPHRO SLIDES TOP 10 NEPHRO SLIDES IN BOARD EXAMS IN BOARD EXAMS

BOARD EXAM SLIDESBOARD EXAM SLIDES

WHAT IS THIS ?WHAT IS THIS ?

WHAT IS THIS ?WHAT IS THIS ?

WHAT IS THIS ?WHAT IS THIS ?

WHAT IS THIS ?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 COMMONEST NEPHRO CASES IN BOARD EXAM – TRICKS AND CLUESBOARD EXAM – TRICKS AND CLUES MOST OF THE CASES CONTAIN ONE SINGLE MOST OF THE CASES CONTAIN ONE SINGLE

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

LOOK FOR THAT CLUELOOK FOR THAT CLUE

THIS IS THE M-KASAP TYPE OF QUESTIONSTHIS IS THE M-KASAP TYPE OF QUESTIONS

GLOMERULONEPHRITIS EXAM GLOMERULONEPHRITIS EXAM TRICKS AND CLUESTRICKS AND CLUES

A.RBC CASTS:A.RBC CASTS: 1. MPGN1. MPGN 2.IGA2.IGA 3.POST STREP GN3.POST STREP GN 4.SLE NEPRITIS4.SLE NEPRITIS 5.RPGN AS ANCE NEPHRITIDES5.RPGN AS ANCE NEPHRITIDES

CONTINUES CLUESCONTINUES CLUES

A PATIENT WITH GLOMERULAR A PATIENT WITH GLOMERULAR PROTIENUREA AND INCREASED LIVER PROTIENUREA AND INCREASED LIVER ENZYMES IS MPGN DUE TO HEP CENZYMES IS MPGN DUE TO HEP C

A PATIENT OBESE WITH PROTIENUREA IS A PATIENT OBESE WITH PROTIENUREA IS FSGSFSGS

CONTINUECONTINUE

A PATIENT WITH HEROIN ABUSE AND A PATIENT WITH HEROIN ABUSE AND PROTIENUREA IS FSGSPROTIENUREA IS FSGS

A PATIENT WITH PROTIENUREA AND RENAL A PATIENT WITH PROTIENUREA AND RENAL IMPAIRMENT AND FEW + DIPSTICK WITH IMPAIRMENT AND FEW + DIPSTICK WITH LARGR TOTAL 24 HRS PROTIENUREA ID M LARGR TOTAL 24 HRS PROTIENUREA ID M MYELOMAMYELOMA

CONTINUESCONTINUES

A PATIENT ON NSAID AND PROTIENUREA IS A PATIENT ON NSAID AND PROTIENUREA IS MMDMMD

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

CORRECT ANSWER IS ACORRECT ANSWER IS A

CHOLESTEROL EMBOLISATATIONCHOLESTEROL EMBOLISATATION ONE OF THE MOST AND TOP QUESTIONS IN ONE OF THE MOST AND TOP QUESTIONS IN

ARAB-SAUDI-AMERICAN BOARD EXAMSARAB-SAUDI-AMERICAN BOARD EXAMS

SIMPLY EXAMINERS THEY LOVE IT !!!SIMPLY EXAMINERS THEY LOVE IT !!!

I TOLD U LOOK FOR THE CLUE!!I TOLD U LOOK FOR THE CLUE!!WHERE IS THE CLUE HERE ?WHERE IS THE CLUE HERE ?

THE CLUE IS THE TIME OF INCREASE IN CR THE CLUE IS THE TIME OF INCREASE IN CR WHICH IS AFTER 48 HRSWHICH IS AFTER 48 HRS

CONTRAST GIVE U INCREASE CR WITHIN CONTRAST GIVE U INCREASE CR WITHIN FIRST 24 HRS OF THE ANGIO BUT CE THE FIRST 24 HRS OF THE ANGIO BUT CE THE RISE IS AFTER 48 HRSRISE IS AFTER 48 HRS

OTHER CLUES LOW COMPLEMENTS,AND OTHER CLUES LOW COMPLEMENTS,AND HIGH ESRHIGH ESR

CE-CASECE-CASE

ESINOPHILLIAESINOPHILLIA DIGITAL INFARCTSDIGITAL INFARCTS LIVEDO RETICULARISLIVEDO RETICULARIS RETINAL EMBOLI AND HEMORRHAGESRETINAL EMBOLI AND HEMORRHAGES RISK INCREASED BY HEPARINERISK INCREASED BY HEPARINE AS CTDAS CTD PROGNOSIS GRAVE ( NO SINGLE CASE HAS BEEN PROGNOSIS GRAVE ( NO SINGLE CASE HAS BEEN

RECOVEREDRECOVERED

Cr timingCr timing

Cr increase in contrast within first 24 hrsCr increase in contrast within first 24 hrs

Cr increase in embolisation after 24-72 hrsCr increase in embolisation after 24-72 hrs

Cr increase in gentamycine after 7-10 daysCr increase in gentamycine after 7-10 days

All the follwing are true of All the follwing are true of preclampcia EXCEPT :preclampcia EXCEPT :

A. high uric acidA. high uric acid B. high CrB. high Cr C. no urine RBC castsC. no urine RBC casts D. high urine calciumD. high urine calcium E. high urine protienE. high urine protien

36 yrs female known case of SLE 36 yrs female known case of SLE want to become pregnant, what want to become pregnant, what

would u advice her ?would u advice her ? A. the single most important is Cr level at the A. the single most important is Cr level at the

time of conceptiontime of conception B.the single most important is disease activity B.the single most important is disease activity

level at conceptionlevel at conception C.the single most imprtant is protienureaC.the single most imprtant is protienurea D.A AND BD.A AND B E.B AND CE.B AND C

25 OLD MALE COCCAINE ABUSER 25 OLD MALE COCCAINE ABUSER PRESENTED TO ER WITH :PRESENTED TO ER WITH :

VOMITING,HYPERTENTION,AND FEVER WITH VOMITING,HYPERTENTION,AND FEVER WITH DECREASE URINE OUTPUTDECREASE URINE OUTPUT

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

LABSLABS

CBC WBC 7,PLAT 230,Hb 10.6CBC WBC 7,PLAT 230,Hb 10.6 LFT NORMALLFT NORMAL Cr 600 AND ONE MONTH AGO WAS 78Cr 600 AND ONE MONTH AGO WAS 78 Na 137, K 6.8,Ca 1.2,Ph 1.9Na 137, K 6.8,Ca 1.2,Ph 1.9 Uric Acid 600Uric Acid 600 UA POSITIVE FOR BLOOD +++ ON UA POSITIVE FOR BLOOD +++ ON

DIPSTICK,PROT +,RBC 1-5DIPSTICK,PROT +,RBC 1-5

THE MOST LIKELY DX:THE MOST LIKELY DX:

A. RHABDOMYOLYSISA. RHABDOMYOLYSIS B. SBEB. SBE C.TUMOR LYSIS SYNDROMEC.TUMOR LYSIS SYNDROME D.POST INF GND.POST INF GN E.POLYARTERITIS NODOSAE.POLYARTERITIS NODOSA

RHABDOMYOLYSIS-THINGS IN RHABDOMYOLYSIS-THINGS IN EXAM TO REMEMBEREXAM TO REMEMBER

THE COMMONEST CAUSE IS TRUMA-SOLDIER THE COMMONEST CAUSE IS TRUMA-SOLDIER SYNDROMESYNDROME

THE COMMONEST DRUG IS COCCAINETHE COMMONEST DRUG IS COCCAINE OTHER DRUGS HMG-COENZ-RED-INHIBITORS OTHER DRUGS HMG-COENZ-RED-INHIBITORS

AS STATINSAS STATINS THE SINGLE MOST IMPORTANT STEP IN THE SINGLE MOST IMPORTANT STEP IN

MANAG IS IVF AND IVF AND IVFMANAG IS IVF AND IVF AND IVF

COMMON MCQ IN EXAMS-GNCOMMON MCQ IN EXAMS-GN

54 YRS MALE PRESENTED WITH 54 YRS MALE PRESENTED WITH WEAKNESS,DIAZINESS, FOR 4 MONTHSWEAKNESS,DIAZINESS, FOR 4 MONTHS

CBS HB 8GM,WBC 5,PLAT 230CBS HB 8GM,WBC 5,PLAT 230 LFT Na 137,K 6,Ca 2.6,LFT Na 137,K 6,Ca 2.6, U/A DIPSTICK PROTIEN +,BLOOD –U/A DIPSTICK PROTIEN +,BLOOD – MICROSCOPY NO RBC CASTSMICROSCOPY NO RBC CASTS TOTAL 24 HRS PROTIEN 8 GMTOTAL 24 HRS PROTIEN 8 GM

RENAL BX;RENAL BX;

THE MOST LIKELY DX IS ;THE MOST LIKELY DX IS ;

A.AMYLOIDOSISA.AMYLOIDOSIS B.MYELOMA KIDNEYB.MYELOMA KIDNEY C.MEMRANOUS GNC.MEMRANOUS GN D.FSGSD.FSGS E.MINIMAL CHANGE DISEASEE.MINIMAL CHANGE DISEASE

MYELOMA KIDNEY-EXAM MYELOMA KIDNEY-EXAM FAVOURITE FAVOURITE

THE MOST IMPORTANT CLUE IN EXAM IS THE MOST IMPORTANT CLUE IN EXAM IS DIPSTICK URINE NEGATIVE FOR PROTIEN OR DIPSTICK URINE NEGATIVE FOR PROTIEN OR MILD + POSITIVE BUT THE 24 HRS URINE MILD + POSITIVE BUT THE 24 HRS URINE COLLECTION FOR PROTIEN IS MORE THAN 3 COLLECTION FOR PROTIEN IS MORE THAN 3 GM. WHY ?GM. WHY ?

LARGE KIDNEY. WHAT OTHER CAUSES OF LARGE KIDNEY. WHAT OTHER CAUSES OF LARGE KIDNEY ????LARGE KIDNEY ????

TWO TYPES OF MYELOMA KIDNEYTWO TYPES OF MYELOMA KIDNEY

A. TUBULAR WITH LIGHT CHAIN DEPOSITION A. TUBULAR WITH LIGHT CHAIN DEPOSITION AND GIVE U FRACTURED CAST DIAGNOSTIC AND GIVE U FRACTURED CAST DIAGNOSTIC OF MM.THIS TYPE HAS GOOD PROGNOSISOF MM.THIS TYPE HAS GOOD PROGNOSIS

B.LDD-CHARACTERISED BY NODULAR B.LDD-CHARACTERISED BY NODULAR SCELEROSIS AND POOR PROGNOSISSCELEROSIS AND POOR PROGNOSIS

MEMBRANOUS GN-EXAM POINTSMEMBRANOUS GN-EXAM POINTS

THE COMMONEST CAUSE OF RENAL VIEN THE COMMONEST CAUSE OF RENAL VIEN THROMBOSISTHROMBOSIS

THE COMMONEST CAUSE OF NEPHROTIC THE COMMONEST CAUSE OF NEPHROTIC SYNDROME IN ADULTSSYNDROME IN ADULTS

COMPLEMENTS NORMAL,NO RBC CASTSCOMPLEMENTS NORMAL,NO RBC CASTS ASSOCCIATED WITH MALIGNANCY COLONASSOCCIATED WITH MALIGNANCY COLON

MGNMGN

IDIOPATHICIDIOPATHIC SECONDARY TO DRUGS ( ACE,GOLD,PENCILLAMINE )SECONDARY TO DRUGS ( ACE,GOLD,PENCILLAMINE ) INFECTIONS(MALARIA,HEP B)INFECTIONS(MALARIA,HEP B) TREATMENT( ACE,PONTICELLI TREATMENT( ACE,PONTICELLI

PROTOCOL=CHLORAMPUCIL ALTERNATING WITH PROTOCOL=CHLORAMPUCIL ALTERNATING WITH STEROIDS OR IMMURAN STEROIDS OR IMMURAN

RESISTANT USE CYCLOSPORINERESISTANT USE CYCLOSPORINE

PROGNOSIS-THE 25 % DISEASEPROGNOSIS-THE 25 % DISEASE

25 % COMPLETE RECOVERY25 % COMPLETE RECOVERY 25 % PARTIAL RECOVERY25 % PARTIAL RECOVERY 25 % ESRD25 % ESRD 25 % RELAPSE ON AND OFF25 % RELAPSE ON AND OFF

FSGS-EXAM QUESTIONSFSGS-EXAM QUESTIONS

THE COMMONEST QUESTIONS IS CAUSES THE COMMONEST QUESTIONS IS CAUSES OR A CASE WHICH TELL U THE CAUSEOR A CASE WHICH TELL U THE CAUSE OBESE PATIENT WITH PROTIENUREA IS FSGSOBESE PATIENT WITH PROTIENUREA IS FSGS A PATIENT WITH HIV THE COOMNEST RENAL A PATIENT WITH HIV THE COOMNEST RENAL

BX FINDING IS COOLAPSING FSGSBX FINDING IS COOLAPSING FSGS A PATIENT ON HEROINE OR DRUG ABUSER IS A PATIENT ON HEROINE OR DRUG ABUSER IS

FSGS OR INF-@FSGS OR INF-@

FSGSFSGS

A PATIENT WITH SINGLE KIDNEY AND A PATIENT WITH SINGLE KIDNEY AND PROTIENUREA IS FSGSPROTIENUREA IS FSGS

A PATIENT WITH REFLUX HAS FSGSA PATIENT WITH REFLUX HAS FSGS STEROIDS CAN INDUSE REMISSION IN 40 % STEROIDS CAN INDUSE REMISSION IN 40 %

OF CASESOF CASES IT IS THE HIGHEST AND FASTEST IT IS THE HIGHEST AND FASTEST

RECURRENCE OF RENAL TX WITH MPGNRECURRENCE OF RENAL TX WITH MPGN

HIV NEPHROPATHYHIV NEPHROPATHY

POINTS TO REMEMBER IN EXAMS:POINTS TO REMEMBER IN EXAMS: 1.LARGE KIDNEY1.LARGE KIDNEY 2.CYSTIC TUBULAR DILATATION2.CYSTIC TUBULAR DILATATION 3.ENDTHELIAL CYTOPLASMIC 3.ENDTHELIAL CYTOPLASMIC

RETICLOTUBULAR STRUCTURES ON EMRETICLOTUBULAR STRUCTURES ON EM 4.COLLAPSING FSGS IS THE COMMONEST 4.COLLAPSING FSGS IS THE COMMONEST

VARIETYVARIETY

MCD-EXAM QUESTIOSMCD-EXAM QUESTIOS

NSAID IS THE ONLY DRUG KNOWN TO CAUSE NSAID IS THE ONLY DRUG KNOWN TO CAUSE MCD WITH INF-@MCD WITH INF-@

ALL MALIGNANCY ASSOCIATED WITH ALL MALIGNANCY ASSOCIATED WITH MEMBRANOUS GN EXCEPT ONE MLIGNANCY MEMBRANOUS GN EXCEPT ONE MLIGNANCY ASSOCIATED WITH MCD DO U KNOW WHAT IT ASSOCIATED WITH MCD DO U KNOW WHAT IT IS ????????????IS ????????????

Hodgkin’s lymphoma.Hodgkin’s lymphoma.

MCD-EXAM POINTSMCD-EXAM POINTS

• IN A PATIENT WITH MCD WHO IS NOT RESPONDING TO IN A PATIENT WITH MCD WHO IS NOT RESPONDING TO ADEQUATE COURSE OF STEROIDS THE MOST LIKELY ADEQUATE COURSE OF STEROIDS THE MOST LIKELY CAUSE IS FSGS SO DO RENAL BXCAUSE IS FSGS SO DO RENAL BX

• THE MOST IMPORTANT POINTS ABOUT MCD IS THISTHE MOST IMPORTANT POINTS ABOUT MCD IS THIS

• IN CHILDREN A COURSE OF 8 WEEKS STEROIDS IS IN CHILDREN A COURSE OF 8 WEEKS STEROIDS IS ADEQUATE TO INDUSE REMISSIONADEQUATE TO INDUSE REMISSION

BUT IN ADULTS THE STORY IS BUT IN ADULTS THE STORY IS DIFFERENTDIFFERENT

IN ADULTS DO NOT LABEL THE PATIENT AS IN ADULTS DO NOT LABEL THE PATIENT AS STEROIDS RESISTANT UNLESS U GIVE 12 STEROIDS RESISTANT UNLESS U GIVE 12 WEEKS OF STEROIDS WEEKS OF STEROIDS

REMEMBER AT LEAST 12 WEEKSREMEMBER AT LEAST 12 WEEKS DO U KNOW THE DIFFERENCE BETWEEN DO U KNOW THE DIFFERENCE BETWEEN

STEROIDS DEPENDENT AND STEROIDS STEROIDS DEPENDENT AND STEROIDS RESISTANT AND STEROIDS RELAPSERRESISTANT AND STEROIDS RELAPSER

MPGN-EXAM POINTSMPGN-EXAM POINTS

THE HIGHEST RECURRENCE OF DISEASE IN THE HIGHEST RECURRENCE OF DISEASE IN TX ( 80 % )TX ( 80 % )

THE COMMONEST CAUSE OF MPGN IN THE THE COMMONEST CAUSE OF MPGN IN THE WORLD NOW IS …………… Hepatitis C ……………WORLD NOW IS …………… Hepatitis C ……………

CRYOGLOBULINEMIA IS IMPORTANT CAUSECRYOGLOBULINEMIA IS IMPORTANT CAUSE

FREQUENT AND COMMON BOARD FREQUENT AND COMMON BOARD EXAM QUESTION IS THIS ONEEXAM QUESTION IS THIS ONE

54 YRS MALE PRESENTED WITH HEAVY 54 YRS MALE PRESENTED WITH HEAVY PROTIENUREA OF 7GMPROTIENUREA OF 7GM

HIS LFT IS ABNORMALAHIS LFT IS ABNORMALA THE RENAL BIOBSY WILL THE RENAL BIOBSY WILL

SHOW…………………………….SHOW…………………………….

RPGN-THE MOST FREQUNT RPGN-THE MOST FREQUNT QUESTION COMES IN EXAMSQUESTION COMES IN EXAMS

IT IS A MEDICAL EMERGENCYIT IS A MEDICAL EMERGENCY IN FACT IT IS THE ONLY GN THAT IS IN FACT IT IS THE ONLY GN THAT IS

EMERGENCYEMERGENCY IT CAN KILL THE KIDNEY IN 72 HRS IF U DID IT CAN KILL THE KIDNEY IN 72 HRS IF U DID

NOT ACTNOT ACT U START RX EVEN BEFORE THE BX RESULTU START RX EVEN BEFORE THE BX RESULT

CAUSES;CAUSES;

WEGNERSWEGNERS PANPAN CHURG-STRAUSSCHURG-STRAUSS ANTI-GBMANTI-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-ANCAP-ANCA

WEGNERSWEGNERS MICROSCOPIC POLYANGIOPATHYMICROSCOPIC POLYANGIOPATHY CHURG-STRAUSSCHURG-STRAUSS IDIOPATHIC RPGN IN THE ELDERLYIDIOPATHIC RPGN IN THE ELDERLY

REVERSAL OF RENAL FUNCTION IN REVERSAL OF RENAL FUNCTION IN ANTI-GBM DISEASE(GODPASTUER)ANTI-GBM DISEASE(GODPASTUER)

IF Cr LESS THAN 550IF Cr LESS THAN 550 IF PATIENT NOT YET STARTED ON DIALYSISIF PATIENT NOT YET STARTED ON DIALYSIS IF PLASMAPHRESIS STARTED EARLYIF PLASMAPHRESIS STARTED EARLY

BEST RX FOR GODPASTUREBEST RX FOR GODPASTURE

PLASMAPHRESISPLASMAPHRESIS

PULSE IV STEROIDSPULSE IV STEROIDS

BEST RX FOR WEGNERSBEST RX FOR WEGNERS

PULSE IV STEROIDSPULSE IV STEROIDS

CYCLOPHOSCYCLOPHOS

PLASMAPHRESISPLASMAPHRESIS

C-ANCA-ONLY WEGNERSC-ANCA-ONLY WEGNERS

THE MOST IMPORTANT SLIDE IN THE MOST IMPORTANT SLIDE IN GLOMERULONEPHRITISGLOMERULONEPHRITIS

ANY CASE IN THE EXAM MENTION UA ANY CASE IN THE EXAM MENTION UA CONTAIN RBC-CASTCONTAIN RBC-CAST

THERE ARE ONLY 5 DDX IN MEDICINETHERE ARE ONLY 5 DDX IN MEDICINE

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

CAUSES OF RBC-CAST THIS IS CAUSES OF RBC-CAST THIS IS CALLED ACTIVE URINE SEDIMENTCALLED ACTIVE URINE SEDIMENT

1. MPGN1. MPGN 2.IGA NEPHROPATHY2.IGA NEPHROPATHY 3.POST-INFECTIOUS GN AS POST-3.POST-INFECTIOUS GN AS POST-

STREPTOCOCCAL GNSTREPTOCOCCAL GN 4.SLE4.SLE 5.RPGN5.RPGN

WHAT IS THE SINGLE WHAT IS THE SINGLE MOST IMPORTANT TEST MOST IMPORTANT TEST

TO DIFFRENTIATE TO DIFFRENTIATE BETWEENBETWEENPRERENAL AND POSTRENAL PRERENAL AND POSTRENAL

AZOTEMIA ( ATN ) ??AZOTEMIA ( ATN ) ??

IT IS FENAIT IS FENA

PROXIMAL RTA

MA WITH NORM AGURINE PH < 6 ACIDIFY THE URINEDISTAL RTA ALWAYS URINE PH >6DISTAL 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

HYPONATREMIAHIGH 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 22 yrs male found comatose and his friends mention that he had friends mention that he had problems with his wife and problems with his wife and

attempted suicide and his labs;attempted suicide and his labs;Na 140,k 5,cl 95,CO2 10,GLUCOSE Na 140,k 5,cl 95,CO2 10,GLUCOSE

7,PLASMA OSMOL 325,BUN 137,PLASMA OSMOL 325,BUN 13

PH 7.1,PCO2 24,PO2 85PH 7.1,PCO2 24,PO2 85

WHAT ACID BASE DISTURBANCE ?WHAT ACID BASE DISTURBANCE ? IS IT SIMPLE OR MIXED ?IS IT SIMPLE OR MIXED ? WHAT IS THE DX ?WHAT IS THE DX ?

Expected PCO2 = 1.5 X HCO3 + 8 ( + Expected PCO2 = 1.5 X HCO3 + 8 ( + OR – 2 )OR – 2 )

MA WITH HIGH AGMA WITH HIGH AG EXP PCO2 IS 21 – 25EXP PCO2 IS 21 – 25 MA POISONINGMA POISONING

5-DAYS LATER HIS ABG :5-DAYS LATER HIS ABG :

PH 7.2PH 7.2 HCO3 16HCO3 16 PCO2 45PCO2 45

WHAT ACID BASE IS THIS ?WHAT ACID BASE IS THIS ?

EXP PCO2=1.5 X 16 + 8=32EXP PCO2=1.5 X 16 + 8=32

BUT PCO2 IS 45 SO THIS IS MIXED MA + RESP BUT PCO2 IS 45 SO THIS IS MIXED MA + RESP ACIDOSISACIDOSIS

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.

identical to those of patients who are on thiazide diuretics

Gitelman's syndrome

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 abuseBarttar/gitelman syndromeWhy ???

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 DISEASE-MKSAP 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 PointIn patients with chronic kidney disease,

iron deficiency anemia should be corrected before initiation of an erythropoiesis-stimulating agent .

Key PointIn patients with symptomatic, acute

hyponatremia, rapid normalization of the extracellular fluid osmolality with

hypertonic saline is indicated .

Key PointAdherence 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 PointObstructive 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 PointThe 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 PointAngiotensin receptor antagonists and

angiotensin-converting enzyme inhibitors are contraindicated during

pregnancy.

Key PointIn 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 PointIn 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 PointThe most common cause of HIV-

associated nephropathy is collapsing focal segmental glomerulosclerosis, which is characterized by massive

proteinuria .

Key PointCorticosteroid 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 PointLithium-induced nephrotoxicity may

manifest as nephrogenic diabetes insipidus and typically progresses slowly .

Key PointIsopropyl 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 PointAmbulatory blood pressure monitoring

is the gold standard for diagnosing white coat hypertension .

Key PointProximal (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 PointThe 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 PointThe most important risk factor for

intracranial aneurysm in patients with autosomal-dominant polycystic kidney

disease is a family member with an intracranial aneurysm

Key PointChronic kidney disease is the most

likely diagnosis in patients with elevated serum creatinine levels and

proteinuria early in pregnancy .

Key PointImmune complex–mediated glomerular

nephritis is characterized by hypocomplementemia and dysmorphic

erythrocytes and erythrocyte casts seen on urinalysis .

Key PointDietary 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 protein-creatinine ratio of 4 to 8 mg/mg and normal

kidney function .

Key PointKidney 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 PointAlkalinization of the urine with potassium citrate therapy to obtain a urine pH above

6.0 decreases the risk of recurrent uric acid stones .

Key PointCerebral 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 PointManifestations 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 PointSalicylate toxicity is a common cause

of mixed anion gap metabolic acidosis and respiratory alkalosis .

Key PointThe 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 PointThe gold standard for diagnosing

renovascular hypertension is intra-arterial digital subtraction

angiography .

Key PointIn 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 PointDiagnosis 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 PointKidney manifestations of sarcoidosis

include interstitial nephritis with granuloma formation,

hypercalciuria, nephrocalcinosis, and various glomerular diseases .

Key PointThe treatment of choice for

pheochromocytoma is surgical resection .

Key PointPrerenal 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 PointNephrostomy 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 end-stage kidney disease.

associated with elevated serum parathyroid hormone and alkaline phosphatase levels, hyperphosphatemia, and hypocalcemia.

Key PointAcute 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 PointUse of tacrolimus and another

cytochrome P450 3A4 inhibitor can cause tacrolimus toxicity, which may

lead to acute kidney dysfunction .

Erythromycin

Key PointSurgical 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 PointPercutaneous 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%.