BRAIN AND THE KIDNEY CROSS TALK

1. Dr Ayman Seddik , MD
ASS.PROF.NEPHOLOGY
AIN SHAMS UNIVERSITY
Brain – kidney
Cross talk

2. Dr Ayman Seddik , brain - kidney cross talk

3. I) INTRODUCTION
II) ACUTE KIDNEY INJURY IN BRAIN INJURUED
PATIENTS
III) CEREBRAL DYSFUNCTION IN ACUTE KIDNEY
INJURY
OUTLINE :
Dr Ayman Seddik , brain - kidney cross talk

4. Dr Ayman Seddik , brain - kidney cross talk
I) INTRODUCTION

5. 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.
Dr Ayman Seddik , brain - kidney cross talk

6. Dr Ayman Seddik , brain - kidney cross talk
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.

7. Dr Ayman Seddik , brain - kidney cross talk

8. Dr Ayman Seddik , brain - kidney cross talk

9. Dr Ayman Seddik , brain - kidney cross talk
I) ACUTE KIDNEY INJURY IN
BRAIN INJURY PATIENTS

10. Dr Ayman Seddik , brain - kidney cross talk
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

11. Dr Ayman Seddik , brain - kidney cross talk
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

12. Dr Ayman Seddik , brain - kidney cross talk
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

13. Dr Ayman Seddik , brain - kidney cross talk
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.

14. Dr Ayman Seddik , brain - kidney cross talk
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
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.

15. Dr Ayman Seddik , brain - kidney cross talk
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
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.

16. Brain injury and the kidney
Dr Ayman Seddik , brain - kidney cross talk
Dilip K. Kulkarni, kidney in acute brain injury Journal of Neuroanaesthesiology and Critical Care
| Vol. 3 • Supplement 1 • 2016 |

17. Dr Ayman Seddik , brain - kidney cross talk
CONTRIBUTING FACTORS TO AKI :
HEMODYNAMIC INSTABILITY
USE OF MANNITOL
ANTIBIOTICS FOR ASSOCIATED SEPSIS
RADIOCONTRAST MEDIA , CONTRAST INDUCED
NEPHROPATHY

18. Dr Ayman Seddik , brain - kidney cross talk
I) CEREBRAL DYSFUNCTION
IN ACUTE KIDNEY INJURY

19. Dr Ayman Seddik , brain - kidney cross talk

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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.

21. Dr Ayman Seddik , brain - kidney cross talk
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.

22. Dr Ayman Seddik , brain - kidney cross talk
AKI
RENAL SYMPATHETIC
OVERACTIVITY
HYPERTENSION ISCHEMIC INJURY AND EDEMA
OF MEDULLA AND CEREBELLUM
POSTERIOR REVERSIBLE
ENCEPHALOPATHY SYNDROME

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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 ??

29. Dr Ayman Seddik , brain - kidney cross talk
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.

30. Dr Ayman Seddik , brain - kidney cross talk
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.

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PERITONEAL DIALYSIS
More physilogical in fluid
and solute removal
All have low sodium and
higher glucose
concentration
May exacerbate brain
edema

32. Dr Ayman Seddik , brain - kidney cross talk
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.

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