Hepatorenal syndrome

It is diagnosed when acute liver failure or chronic liver disease is already established but

Not simultaneously occurred.

Sepsis or bacteremia must be ruled out and no diretic has been given recently. There should

No recent use of nephrotoxic agent i.e ACE I, ARB, Nsaids, Aminoglycoside etc.

There are two types of HRS established for the sake for understaining and different prognostic

Value.  Typer 1 is manifested for rapidly rise of creatinine usally along with high billirubine and

Prothrombin time. Patients usually die in 2 weeks when left untreated. While in Type 2 there is

Gradual rise of serum creatinine especially in setting of Ascitis which is resistent  to diuretics.

Patients survive upto to 4 to 6 month in case of no treatement offered.

Orthotopic liver transplantion is the treatment of choice but before that paients must be offered

Vasoconstrictive therapy with albumin infusion.

Choice of vasoconstrive therapy are:  Octreotide 4 to 6 mg in TDS which can be increased to 12 mg per

Day. Along with albumin 1 to 1.5 mg per kg for days.

Others options are ocreotide, vasopressin , norepinephrine, midodrine.

Surgical option is TIPS . It is Transhepatic portosystemic shund, and it is an adjuvant.

Case scenario

30 year with history of recurrent renal stone. Analysis of stone came out to be calcium oxalate.

There is no family history of renal stone. IVP shows linear striatiation of papilla and occasionally

Medullary cystic collection of contrast and calcium. His serum chemistry:

Na 139

K   4.0

Cl  109

Hco 19

s.creatine  1.1

Urine Ph 5.8

Arterial Ph 7.37

Arterial Pco 34

Q.     what is the kidny disease?

          What is the acid base abnormality?

         What is the treatment?

Answere:

            Patient has medullary sponge kidney.

            It is complicated by hypercaciruea and metabolic acidosis which is normal

            Anion gap and positive anion gap type.

          In one fouth of medulary sponge kidny patients renal stone are formed.

          Oral alkali thrapy with bicarbonate or citrate salt can be given.

         Thiazide diruretic can be tried.

       Patient is encourage to increase oral fluid so that about 2 to 2.5 liter urine out put 

       Can be maintained.

       Sodium restriction up to not more than 2 gm in 24 hour.

       Proteins should be not more than 1 gm/kg /day.

 

Case discussion

65 year male recently got bed restricted due to generalized weakness following anorexia and vomiting.

He has been using lithium carbonate for his manic-depressive illness for some 15 years.

On examination he is lethargic but able to communicate, Temp: 101f, pulse 124bpm and respiratory rate 16 /min. Blood pressure 100/60 lying and 70/40 on sitting.

Investigation: Lithium 1.5 mmole/lit;  Urea 20mg/dl and S. creatinine 1.3mg/dl. Na 169 ,  Ca 2.3mmole/l.

Glucose 4mmole; urine osmolality 240.

Give probable reason for patients hypernatremia, polyurea and polydipsia?

This patient has developed nephrogenic diabetes inspidus due to prolong use of lithium for his

Manic-depressive illness. Lithium block the action of ADH as well as adenylate cyclase in collecting duct

, thereby excessive water excretion or we can say decreased water absorption has led to increased serum osmolality and decreased urine osmolality. In this way thrist mechnism is stimulated to compensate increased serum osmolality.

\

Common Drugs causing nephrogenic diabetes inspidus:

Lithirm

Amphotericin B

Demeclocycline

Polyurea with headache

29 year woman with 1 month history of headache , increased thrist and urinary frequency.
Urinary out put over 24 hours was 8 liters.Fluid deprivation test was performed with following
results:

 Time                              Serum Osm                  Urine Osm                    Serum ADH             Urine output

Baseline                           144                              80                                 2                                  -

1 hour                               147                             80                                  2                              600

2 hour                               150                              80                                  2                               500


Q.        What is the diagnosis?
Q.         Treatment?


Answere:    This patient has central diabetic inspidus and his defect seems to be severe.The D/D should include both central and nephrogenic dI, as well psychogenic polydipsia and diuretic use.

Desmopressin( Vasopressin) is the prefered teatment.








Vasopressin

Urinary Anion Gap

In a patient with non-anion gap metabolic acidosis, calculating the urine anion gap can help differentiate between diarrhea and renal tubular acidosis (RTA) as the etiology.

 

A. What is the urine anion gap and how is it calculated?

 

B. In the following case, please determine if the patient has a non-anion gap metabolic acidosis due to diarrhea or RTA:

 

A 24 year old male dancer comes to attention due to a low serum bicarbonate on routine blood work. Additional results include:
Serum: Na 140 meq/L, K 3 meq/L, HCO3 14 meq/L, Cl 116 meq/L
Urine: Na 50 meq/L, K 30 meq/L, Cl 40 meq/L.


Answere:

Urine anion gap is calculated by subtracting the urine concentration of chloride(anions) from the concentrations of sodium plus potassium (cations):

= Na⁺ + K⁺ − Cl⁻

where the concentrations are expressed in units of milliequivalents/liter (mEq/L).

In contrast to the serum anion gap equation, the bicarbonate is excluded. This is because urine is acidic, so the bicarbonate level would be negligible.

Urine anion gap is an 'artificial' and calculated measure that is representative of the unmeasured ions in urine. Usually the most important unmeasured ion in urine isNH₄⁺.

• A positive urine anion gap suggests a low urinary NH₄⁺ (e.g. renal tubular acidosis).
• A negative urine anion gap suggests a high urinary NH₄⁺ (e.g. diarrhea).