Brain kidney cross talk final 2016

Dr Ayman Seddik , MD

ASS.PROF.NEPHOLOGY

AIN SHAMS UNIVERSITY

Brain – kidney

Cross talk

Dr Ayman Seddik , brain - kidney cross talk

I) INTRODUCTION

II) ACUTE KIDNEY INJURY IN BRAIN INJURUED

PATIENTS

III) CEREBRAL DYSFUNCTION IN ACUTE KIDNEY

INJURY

OUTLINE :



I) INTRODUCTION

impulses from central

nervous system (CNS)

regulate

1. renal blood flow

2. glomerular filtration

rate

3. renal sodium handling

On the other hand,

impulses originating from

the kidney are carried via

unmyelinated and thinly

myelinated fibres to the CNS

and the contralateral kidney

to

1. regulate CNS activity

2. coordinate renal

sodium handling.



Both Brain and

kidney have a

common feature of a

tight

auto-regulatory

mechanism that

maintains constant

blood flow over a

wide range of blood

pressures

YET , It is

unclear whether

these mechanisms

are interconnected.


I) ACUTE KIDNEY INJURY IN

BRAIN INJURY PATIENTS


Renal problems can occur

in various acute cerebral

insults such as :

1. cerebral ischaemic

stroke

2. subarachnoid

3. Haemorrhage

4. intracerebral

haemorrhage

5. head injury

6. white matter lesions.

The brain injury can influence

the kidney function by

following main mechanisms:

• Neuro-inflammation

• increased

neuro-sympathetic activity

• hypothalamo-pituitary axis


Neuro-inflammation:

Brain injury activates an inflammatory response, the intensity of which

is related to the degree of the primary injury and subsequent secondary

insults

The complex cascade of

inflammatory events following brain injury is mediated by

the production and activation of

* Complements

* cytokines

* adhesion molecules

* other multifunctional peptides.

Cells of the CNS are an abundant source of inflammatory

Mediators and CNS expression of pro-inflammatory

cytokines and complement components leads to

recruitmentof neutrophils and monocytes (macrophages) across

the blood–brain barrier (BBB) and enhancement of the

established neuro-inflammation


Intracranial inflammatory mediators pass into the systemic circulation via a dysfunctional BBB and elevated levels of cytokines are present in plasma as well as cerebrospinal

fluid after brain injury.

They mediate systemic changes such as

*Fever

*Neutrophilia

* muscle breakdown

*alteredamino acid metabolism

*production of hepatic acute phasereactants

*altered endothelial permeability


IMMUNODEPRESSION

INTRACRANIAL HYPERTENSION

INCREASED INTERLEUKIN 10 (IL10)

FROM PERIPHERAL MONONCYTES

ENDOGENOUS CATECHOLAMINES

SELECTIVE INHIBITION OF CELLULAR

IMMUNITY THROUGH IMMUNE INHIBITORY

PATHWAY

STRESS INDUCED METABOLIC RESPONSE

INFECTIONS

SYSTEMIC INFLAMMATORY RESPONSE

MULTISYSTEM ORGAN DYSFUNCTION AND

ACUTE KIDNEY INJURY

Diagram Based on ., Freeman WD, Wadei HM. A brain-kidney connection: The

delicate interplay of brain and kidney physiology. Neurocrit

Care 2015;22:173-5.


INCREASED SYMPATHETIC ACTIVITY

INCREASED NA REABSORPTION

REDUCED RENAL PERFUSION

REDUCED GFR

AKI

SUSTAINED SEVERE HYPERTENSION

WILL LEAD TO RED BLOOD CELL FRAGMENTATION

AND GLOMERULAR MICROTHROMBI

INCREASED CATECHOLAMINES IN

VISCERAL SYMAPATHETIC NERVOUS SYSTEM



Care 2015;22:173-5.


Brain injury

Hypothalamic – pituitary Acess

DISTURBED ADH (Vasopressin) secretion

ADH

SECRETION

SIADH

ADH

CRANIAL DIABETUS INSIPIDUS

DISTURBED NA HANDLING IN RENAL

TUBULES

CEREBRAL SALT WASTING SYNDROME



Care 2015;22:173-5.

Brain injury and the kidney


Dilip K. Kulkarni, kidney in acute brain injury Journal of Neuroanaesthesiology and Critical Care

| Vol. 3 • Supplement 1 • 2016 |


CONTRIBUTING FACTORS TO AKI :

HEMODYNAMIC INSTABILITY

USE OF MANNITOL

ANTIBIOTICS FOR ASSOCIATED SEPSIS

RADIOCONTRAST MEDIA , CONTRAST INDUCED

NEPHROPATHY


I) CEREBRAL DYSFUNCTION

IN ACUTE KIDNEY INJURY


ALTER NEURONAL CELL PROTEIN TRANSCRIPTION AND NEURONAL ACTIVATION

DISTURBED CERBRAL FUNCTION

DISRUPTION OF BLOOD BRAIN BARRIER

ENDOTHELIAL INJURY

STIMULATION OF INFLAMMATORY AND COAGULATION CASCADE WITHIN THE BRAIN

AKI

SYSTEMIC INFLAMMATORY RESPONSE INCREASED URIC ACID

MARKER AND MEDIATOR OF RENAL ISCHEMIC INJURY

RELEASE OF PROINFLAMMTORY MEDIATORS

ENDOTHELIN , LARGE MULTIMER OF VWF , IL 8 , ANGIOTENSIN 2

Diagram based on data from , Ratliff BB, Rabadi MM, Vasko R, Yasuda K, Goligorsky MS: Messengers

without borders: mediators of systemic inflammatory response in AKI.

J Am Soc Nephrol 2013, 24:529–536.


AKI… DISTURBED NEUROTRANSMITTERS METABOLISM

AKI.. METABOLIC ACIDOSIS …INHIBITION OF CEREBRAL NEURONAL FUNCTIONS

DISRUPT CNS FUNCTIONS

*IMPAIRED LOCOMOTOR FUNCTIONS

*Wide CLINICAL PRESENTATION FROM HYPEREXCITABLE STATE ……..to COMA

Diagram based on data from , Ratliff BB, Rabadi MM, Vasko R, Yasuda K, Goligorsky MS: Messengers

without borders: mediators of systemic inflammatory response in AKI.

J Am Soc Nephrol 2013, 24:529–536.


AKI

RENAL SYMPATHETIC OVERACTIVITY

HYPERTENSION ISCHEMIC INJURY AND EDEMA OF MEDULLA AND CEREBELLUM

POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME


RRT IN SETTING OF BRAIN INJURY AND AKI

IMPROVE ENCEPHALOPATHY BY REMOVING UREAMIC

TOXINS AND TOXIC DRUGS

BUT RAPID OSMOTIC SHIFT MAY PARADOXICALLY

DETERIORATE THE CASE AND CAUSE

BRAIN EDEMA

WHICH MODALITY IS THE BEST ??


1) INTERMITTENT HEMODIALYSIS

READILY AVAILABLE

EFFICIENT FLUID AND DRUGS REMOVAL

BUT

USING THE HIGH EFFICIENCY BICARBONATE DIALYSIS WILL LEAD TO RAPID CHANGES IN BLOOD (PH) AND AS BICARBONATE MOVES

SLOWLY FROM ECF TO ICF

PARADOXICAL INTRACELLULAR ACIDOSIS RESULTS

AND BRAIN EDEMA DEVELOP

Silver SM: Cerebral edema after rapid dialysis is not caused by an

increase in brain organic osmolytes. J Am Soc Nephrol 1995, 6:1600–1606.


Chen CL, Lai PH, Chou KJ, Lee PT, Chung HM, Fang HC: A preliminary

report of brain edema in patients with uremia at first hemodialysis:

evaluation by diffusion-weighted MR imaging. Am J Neuroradiol 2007,

28:68–71.


PERITONEAL DIALYSIS

More physilogical in fluid and solute removal

All have low sodium and higher glucose concentration

May exacerbate brain edema


CRRT

WILL ANSWER THE QUESTION

SLOW CORRECTION OF ACIDEMIA

NO RAPID OSMOTIC SHIFT

NO RAPID ELECTOLYTES CHANGES

LESS POSSIBILITY OF BRAIN EDEMA

NOT AVAILABLE IN ALL SETUP

Davenport A: Continuous renal replacement therapies in patients with

acute neurological injury. Semin Dial 2009, 22:165–168.

Brain kidney cross talk final 2016

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