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AN INTERESTING CASE OF HYPOKALEMIA

GUIDANCE: DR VEDAVATHI. R

DR SUNIL.

DR MANASA

DR RAKSHIT

PRESENTER: DR ANKIT P BHOJANI

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PATIENT DETAILS

Name : Mr B.

Age : 58

Sex : Male

Occupation : Farmer

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PRESENTING COMPLAINTS

Chief complaints:

• Fever since 1 month

• Generalised weakness 15 days

History of presenting illness:

•A 58 year old patient with no

previous known comorbidities was

admitted to the hospital with

complaints of fever since one

month which was insidious in onset

, low grade , not associated with

chills , no diurnal variation .

• History of generalised

weakness since 15 days

• No other significant history.

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PAST AND PERSONAL HISTORY

Not a known case of type 2 DM, hypertension

No history of tuberculosis , asthma , epilepsy in past

No previous hospital admissions for the same

Nothing significant( no use of any OTC medication or

alternate medicine ).

Family history Nothing significant

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General physical examination

Elderly male conscious cooperative oriented to time place person

No pallor, icterus ,cyanosis, clubbing, lymphadenopathy

Pulse :62/min , regular ,normal volume

Blood pressure:126/70 mm/hg

Temperature: a febrile

RR: 16/ min

BMI: 22.4 kg/m2

Head to toe examination : nothing significant

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SYSTEMIC EXAMINATION

RS: bilateral air entry equal , NVBS, no added sounds

CVS: S1 ,S2 heard

No added sounds/murmurs

Per abdomen : soft non tender, no organomegaly

CNS: Conscious , oriented , no focal neurological deficit

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INVESTIGATIONS

Hb : 12.6 mg/dl

TC : 12800 cells/cc

DC : N :84 , L :12 ,M:02

PLATELET:2.73 L

ESR:55

UREA :47

CREATININE:0.8

ELECTROLYTES Na:129 meq/L

K:2.8 meq/L

Cl:88 meq/L

RBS :113mg /dl

ECG: sinus rhythm

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LFT-Normal

URINE ROUTINE ALB: nil

GLU: nil

PC: 6-8

EC: 1-2

WIDAL negative

MPQBC negative

HIV non reactive

HBsAg non reactive

BLOOD CULTURE - no growth

URINE CULTURE - E. coli

USG ABDOMEN AND PELVIS:

kidneys normal

grade 2 prostatomegaly with significant post void residual urine

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WORKING DIAGNOSIS

A diagnosis of urinary tract infection with benign

prostatic hypertrophy was made and patient was started

on antibiotics and supportive care.

Evaluation for electrolyte disturbance was

started.

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Follow up investigations

ABG: Metabolic alkalosis

ELECTROLYTES Na:129 meq/L

K: 2.6 meq/L

Cl: 89 meq/L

Urea :39

Creatinine:0.8

Ca-normal

Po4 , uric acid : normal

PSA: Normal

Thyroid profile : normal

ECHO : normal

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DIFFERENTIALS

HYPOMAGNESEMIA

SALT WASTING SYNDROME

TUBULOPATHIES

HYPERALDOSTERONISM

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FURTHER INVESTIGATIONS

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SERUM Mg: 1.6 mg/dl

Serum osmolality: 280 mmol/kg(275-295)

Urine osmolality: 324mOsm/kg(300-900)

Urine sodium : 34mmol/l

urine potassium : 42mmol/l

Electrolytes Na: 138 meq

K: 2.9 meq

Cl: 88 meq

Estimated glomerular filtrate rate 96 ml/min/1.73 m2

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Patient was started on magnesium correction .

Despite the same patient had persistent hypokalemia and hypochloremia

A diagnosis of salt wasting syndrome was made and work up for the same was carried out.

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Serum K(2.8)

Ruled out other causes of hypokalemia

(drugs, nausea , vomiting , diarrhoea)

Urine potassium (42mmol/l)

>20 <20

Renal loss skin and GI loss

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FURTHER INVESTIGATIONS?

1)WORK UP FOR TUBULOPATHIES

2)RULE OUT OTHER CAUSES FOR ELECTROLYTE

DISTURBANCES

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WORK UP FOR TUBULOPATHY

24 hour Urine creatinine : 623 mcg/day(500-2000mcg/day)

24 hour Urine calcium : 1.50 mmOL/day(100-300mmOL/day)

Serum renin : normal

Serum aldosterone: normal

Serum cortisol: 6mcg/dl

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TTKG(17.03)

>4 <2

Distal excretion

Increased tubular flow

Blood pressure

Low /normal High

Abg(alkalosis) acidosis

Rennin –aldosterone axis

Urine chloride

high A high A

Low R high R

>20 <10

1 HYPERALDOSTERONISM 2 HYPERALDOSTERONISM

Urine calcium /creatinine

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Urine calcium /creatinine

>0.20(BARTERS) <0.15(GITLEMANNS)

Further work up was done as most cases of gitelmanns are

associated with sjogrens syndrome , but patient had no clinical

symptoms

ANA with profile negative.

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FINAL DIAGNOSIS

1)Gitlemanns syndrome

(idiopathic adult gitlemanns syndrome)

2)Urinary tract infection

3)Benign prostatic hypertrophy (grade 2)

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REASON FOR PRESENTING

Gitelman syndrome is a rare syndrome that affects males and females in equally. The disorder occurs in approximately 1 in 100,000 individuals.

Majority of the cases present in early childhood or adolescents.

Here we present a case of adult idiopathic gitelmanssyndrome presenting in the 5th decade

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FOLLOW UP

Subsequently on initial follow up examinations he was found to have normal serum electrolyte profile and had no symptoms .

Patient was advised for regular follow up and advised to continue oral potassium and magnesium supplementation .

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Patient had no further symptoms or generalised weakness an is currently on daily oral supplementation of potassium and magnesium

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AT ADMISSION AT FOLLOW UP

SERUM K 2.8 2.6 3.1 3.9

SERUM Mg 1.6 1.9

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GITLEMANNS SYNDROME

•Also known as familial hypokalemia-hypomagnesemiais a rare genetic disorder in which there is a specific defect in kidney function

•This defect impairs kidneys ability to reabsorb salt and causes changes in various electrolyte concentrations .

•The electrolytes affected primarily are potassium , sodium , chloride , magnesium , calcium

•Like barters gittlemanns is a salt wasting nephropathy .

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Most cases of Gitelman syndrome are linked to inactivating mutations in the SLC12A3 gene, resulting in a loss of function of the thiazide-sensitive sodium-chloride co-transporter (NCCT).

This genetic mutation in SLC12A3 is present in 80% of adults with Gitelman syndrome.

This cell membrane protein participates in the control of ion homeostasis at the distal convoluted tubule portion of the nephron.

Loss of this transporter also has the indirect effect of increasing calcium reabsorption in a transcellular fashion.

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TREATEMENT

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Most asymptomatic individuals with Gitelman syndrome can be

monitored without medical treatment.

Potassium and magnesium supplementation to normalize blood levels is

the mainstay of treatment.

Large doses of potassium and magnesium are often necessary to

adequately replace the electrolytes lost in the urine.[1] Diarrhea is a

common side effect of oral magnesium which can make replacement by

mouth difficult but dividing the dose to 3-4 times a day is better

tolerated.

aldosterone antagonists (such as spironolactone or eplerenone)

or epithelial sodium channel blockers such as amiloride can be used to

decrease urinary wasting of potassium.[1]

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THANK YOU

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