End-Stage Renal Failure - pediagenosis
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Friday, May 31, 2019

End-Stage Renal Failure

End-Stage Renal Failure
Classification of renal failure
End-stage renal failure (ESRF), as evidenced by a decline in glomerular filtration rate (GFR) such that function is inadequate for health, is relatively common and the prevalence increases with age. It can be classified in two ways, either, according to its temporal progression, or according to its cause.

Classification by temporal progression
The rapid onset of renal failure over a period of days or weeks is termed ‘acute renal failure’ or ‘acute kidney injury’ (AKI), whereas a decline in GFR occurring over months to years is termed  ‘chronic renal failure’ or ‘chronic kidney disease’ (CKD).
Classification of renal failure by cause
The cause of renal failure can be classified using the terms:
These indicate the anatomical site at which the aetiological factor is acting. For example,  systemic hypotension due to blood loss will compromise  the  renal  blood  flow  and  is  a   ‘pre-renal’  cause  of renal failure. In contrast, inflammatory disease of the glomerulus (glomerulonephritis, GN)   is   a   ‘renal’   cause   of   renal   failure. Enlargement of the prostate causing obstruction to the outflow of urine is a ‘post-renal’ cause of renal failure.

End-Stage Renal Failure, Classification of renal failure, Classification by temporal progression, Acute kidney injury, Classification of renal failure by cause, CKD,

Acute kidney injury
The most common cause of AKI is pre-renal failure, which if left untreated will  progress  to   acute  tubular  necrosis  (ATN). ATN occurs if there  is  persistent  hypotension/hypovolaemia and/or exposure to nephrotoxins or sepsis. It is the cause of 60–80% of cases of AKI. ATN is quite common because the renal tubular blood supply is relatively precarious, so that any drop in blood pressure (secondary to hypovolaemia or reduced peripheral vascular resistance as seen in  sepsis)  can  lead  to  tubular  ischaemia. This is a direct result of the anatomical arrangement of the blood supply, which comes to the tubules only after it has passed  through the glomerular capillary bed. Thus, there is always relative hypoxia in the renal   medulla  compared  with  the  cortex. When the mean arterial  pressure  falls,  there  will  be   a  reduced  blood  flow  into the glomerulus via the afferent arteriole and a consequent fall in  GFR. This prompts an increase in vasoconstriction in the efferent glomerular arteriole in an  attempt to maintain GFR, which will further compromise the blood supply to the medulla, leading to increased  hypoxia  and  tubular  ischaemia.  Tubular cells  are  also very metabolically active,  with a number of energy-requiring electrolyte pumps. All of these factors contribute to  susceptibility to ATN.
Histologically, ATN is manifest as ragged, dying tubular cells, which  lose  their  nuclei  and   begin  to  slough  off  into  the  tubular lumen.  Patients  with  pre-renal  failure  should  be   given  fluid  to restore   intravascular   volume   and   nephrotoxins   (non-steroidal  anti-inflammatory drugs [NSAIDs], gentamicin or ACEi) should be  removed.  ATN usually  recovers   spontaneously,  although  the patient may temporarily require renal replacement therapy (RRT). Some  patients sustain irreversible tubular atrophy and a degree of chronic kidney damage.
Other  causes  of  AKI  include  GNs  (5–10%),  obstruction  (5– 10%), and acute tubulointerstitial  nephritis (TIN) (<5%).
GNs are named according to the appearance of the renal biopsy. For  example,  in  minimal  change GN  there  is  no  abnormality in the biopsy when viewed with a light microscope; in membranous GN   there  is  thickening  of  the  glomerular  basement  membrane. IgA  nephropathy  is  characterised by  the  deposition  of  IgA  in the mesangium, etc. Some primary and secondary GNs commonly present with an acute decline in renal  function, while others commonly result in CKD (see below). GNs presenting as AKI include:
  Primary – pauci immune crescentic GN, anti-glomerular basement membrane disease (Goodpasture’s  disease).
  Secondary    lupus nephritis,  antineutrophil cytoplasmic anti- body (ANCA)-associated  vasculitis.
Patients with acute GN may require RRT as well as treatment for the underlying disease (e.g.  immunosuppression +/–   plasma exchange).  The  success  of  these  treatments  is  variable; some patients partially regain renal function while others become permanently dialysis-dependent.
Acute TIN often occurs as the result of an ‘allergic reaction’ to medications, both prescription drugs such as proton pump inhibitors  or  antibiotics,  and  herbal  remedies.  Renal  biopsy   demonstrates   an   intense   lymphocytic   infiltrate in the interstitium, including numerous eosinophils. Management involves removal of the likely causative agent and the administration of oral corticosteroids  to  reduce  renal  inflammation.  This  usually  results  in  the resolution of acute inflammation, but some patients are left with irreversible  interstitial  fibrosis  and  tubular  atrophy,  which  may contribute to the subsequent development of CKD.

CKD  can  be  completely  asymptomatic  until  its  very  terminal stages. Eventually anaemia  (manifest as tiredness or even congestive cardiac failure), uraemia (resulting in nausea, reduced appetite and confusion), phosphate build-up (leading to itchiness) and/or severe  hypertension  (causing  headache  or  blurred  vision)  may prompt  the  patient  to  seek  medical  attention,  where  a  routine blood test reveals high urea and creatinine due to a reduced GFR. In contrast to AKI, where pre-renal and post-renal causes predominate, the causes of CKD tend to be renal in origin. These include:
  diabetes mellitus with associated diabetic nephropathy
  hypertensive nephropathy
  obstructive uropathy (often secondary to prostatic hypertrophy)
  chronic primary GN, e.g. IgA nephropathy or focal segmental glomerulosclerosis (FSGS)
  chronic secondary GN, e.g. lupus nephritis
 adult polycystic kidney disease (APKD)
  chronic pyelonephritis
  renovascular disease.
CKD is classified into different stages according to the patient’s GFR and the presence of urine dipstick abnormalities. These have allowed  the  development  of  management  guidelines  for  patients with stable CKD, and facilitate the provision of consistent care.

Diseases that recur in the transplant
A number of causes of renal failure may reoccur in the allograft. These include:
  structural problems – bladder outflow obstruction
  renal calculi
  urinary tract infections with associated chronic pyelonephritis
  primary GNs – IgA, FSGS, mesangiocapillary glomerulonephritis (MCGN)
  secondary GNs – ANCA-associated vasculitis, lupus nephritis, diabetic nephropathy.

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