In medicine, hemofiltration, also haemofiltration, is a renal replacement

therapy which is used in the intensive care setting. It is usually used to treat
acute kidney injury (AKI), but may be of benefit in multiple organ dysfunction
syndrome or sepsis. During hemofiltration, a patient's blood is passed
through a set of tubing (a filtration circuit) via a machine to a semipermeable
membrane (the filter) where waste products and water (collectively called
ultrafiltrate) are removed by convection. Replacement fluid is added and the
blood is returned to the patient.
Principle
As in dialysis, in hemofiltration one achieves movement of solutes across a
semi-permeable membrane. However, solute movement with hemofiltration
is governed by convection rather than by diffusion. With haemofiltration,
dialysate is not used. Instead, a positive hydrostatic pressure drives water
and solutes across the filter membrane from the blood compartment to the
filtrate compartment, from which it is drained. Solutes, both small and large,
get dragged through the membrane at a similar rate by the flow of water
that has been engendered by the hydrostatic pressure. Thus convection
overcomes the reduced removal rate of larger solutes (due to their slow
speed of diffusion) seen in hemodialysis.

Complication of RRT

Electrolyte Abnormalities
Electrolyte abnormalities may result from renal disease itself or as an iatrogenic complication. In
a study of potassium disorders in patients with chronic kidney disease, lower estimated
glomerular filtration rate (eGFR), diabetes, and use of ACE inhibitors or angiotensin-receptor
blockers were associated with higher odds of having hyperkalemia. Heart failure and African
American race were factors associated with higher odds of hypokalemia. Serum potassium <4.0
and >5.0 mmol/L were significantly associated with increased mortality risk, but there was no
increased risk for progression to ESRD.
Hyperkalemia
Hyperkalemia is the most common clinically significant electrolyte abnormality in chronic renal
failure. This condition is uncommon when patients with end-stage renal disease (ESRD) are
compliant with treatment and diet, unless an intercurrent illness such as acidosis or sepsis
develops. A history of hyperkalemia requiring treatment or poor compliance with treatment
should lower the threshold for ordering a potassium level.
Serum potassium levels usually should be measured in patients with chronic renal failure or
ESRD who present with a systemic illness or major injury. Serum potassium rises when the
serum is acidemic, even though total body potassium is unchanged. Hyperkalemia is usually
asymptomatic and should be treated empirically when suspected and when arrhythmia or
cardiovascular compromise is present.
Electrocardiography (ECG) may be useful in diagnosis of suspected hyperkalemia. Severely
peaked T waves are a relatively specific finding, although this is not a very sensitive test for
hyperkalemia in the setting of chronic renal failure. Widening of the QRS complex indicates
severe hyperkalemia and must be treated aggressively and rapidly. Similar "hyperacute" T-waves
may be seen early in acute MI.

Hyponatremia, hypocalcemia, and hypermagnesemia

Iatrogenic complications related to fluid administration (fluid overload) or medications are
frequently encountered in patients in renal failure. Dilutional hyponatremia may cause mental
status changes or seizures. Hypocalcemia or hypermagnesemia may cause weakness and life-
threatening dysrhythmias. Neuromuscular irritability is seen with hypocalcemia and may present
as tetany or paresthesia. Hypermagnesemia causes neuromuscular depression with weakness and
loss of reflexes. Acidosis may present as shortness of breath due to the work of breathing from
compensatory hyperpnea.

Dialysis Dysequilibrium Syndrome

Dialysis dysequilibrium syndrome is a common neurologic complication seen in dialysis patients
that is characterized by weakness, dizziness, headache, and in severe cases, mental status
changes. The diagnosis is one of exclusion; a prime characteristic of this syndrome is that it is
nonfocal.

Infection
Patients with an arteriovenous fistula or graft should have the site examined regularly. Vascular
access problems include infections, which are usually manifest with typical signs and symptoms
such as local pain, redness, warmth, or fluctuance. Fever may be present without local signs.
Clotting of the vascular access presents as loss of normal bruit or palpable thrill. There may be
signs or symptoms of distal limb ischemia.

CAPD-associated peritonitis
Peritonitis is common in patients who are being treated with CAPD, occurring approximately
once per patient year. Patients present with generalized abdominal pain, which may be mild, or
complain of a cloudy effluent. Localized pain and tenderness suggest a local process, such as
incarcerated hernia or appendicitis. Severe generalized peritonitis may be due to a perforated
viscus as in any other patient. Fever is often absent.
The diagnosis of CAPD-associated peritonitis is confirmed by culture of effluent dialysate (ie,
peritoneal fluid), which should be ordered before empiric treatment. Presumptive diagnosis is
based on a peritoneal fluid white blood cell (WBC) count of greater than 100/mL or a positive
Gram stain. The effluent is often cloudy when peritonitis is present, and this appearance
accurately predicts elevated WBC counts. In patients without peritonitis, WBC counts of 0-
50/mL with a mononuclear predominance are considered normal. Cell counts are usually much
higher with predominant polymorphonuclear neutrophils (PMNs) when peritonitis is present.
However, some culture-positive specimens have less than 100 WBCs.
Peritoneal dialysis is the most frequent dialysis method in children, and peritonitis is a frequent
complication. Congenital abnormality of the kidney and urinary tract was found to be a
significant risk factor for nosocomial peritonitis in pediatric patients with ESRD undergoing
peritoneal dialysis.
A number of prophylactic strategies have been employed to reduce the occurrence of peritonitis,
including the use of oral, nasal, and topical antibiotics; disinfection of the exit site; modification
of the transfer set used in continuous ambulatory PD exchanges; changes to the design of the PD
catheter implanted; the surgical method by which the PD catheter is inserted; the use of antibiotic
prophylaxis in patients undergoing certain invasive procedures; and the administration of
antifungal prophylaxis to PD patients whenever they are given an antibiotic treatment course.

Hemorrhage
Patients may present after dialysis or minor trauma with bleeding from their vascular access site.
Active bleeding can also occur from the incisional wound of a newly placed fistula or graft. The
bleeding can usually be controlled with elevation and firm but nonocclusive pressure. In the
immediate postdialysis period, protamine may be needed to reverse the effect of heparin
(routinely used in dialysis to prevent clotting). Note that life-threatening bleeding may occur.
Anemia is inevitable in chronic renal failure because of loss of erythropoietin production.
Abnormalities in white cell and platelet functions lead to increased susceptibility to infection and
easy bleeding and bruising. This condition results in fatigue, reduced exercise capacity,
decreased cognition, and impaired immunity.

Vascular access aneurysms or pseudoaneurysms

Aneurysms or pseudoaneurysms may form and progressively enlarge to compromise the skin
overlying the site of venous access. These present as localized swelling, which may be pulsatile,
and are often chronic. A rapid increase in size may indicate active bleeding.

Secrete renin

The regulation of renin release from the kidney is complex. Among the manifold controllers is
the macula densa mechanism, which couples the tubular chloride concentration inversely to the
plasma renin concentration in the rat. This occurs in the thick ascending limb of the tubule of
Henle. Changes in regional renin release in the kidney help to determine the sensitivity of the
tubuloglomerular feedback mechanism, consequently modifying the set point for autoregulation
of renal blood flow.

A second control element is sympathetic nervous discharge to the kidney, which stimulates renin
secretion through -adrenergic receptors on the JGCs. Increased renin secretion in response to -
adreneroceptor stimulation is mediated via the formation of cAMP. Cyclic nucleotides are critical
second messengers that determine renin secretory rate and there seems to exist a common
pathway of stimulating renin secretion via cAMP. Hormones, neurotransmitter, and autacoids
that raise the intracellular production of cAMP enhance renin secretion and augment renin
mRNA levels. Thus, it is unequivocally held that cAMP stimulates renin secretion. In contrast,
the effects of cGMP on renin secretion have been discussed controversially. Some find a
stimulatory action; others have reported an inhibitory effect of cGMP on renin release. Chiu and
Reid demonstrated an important interaction between cAMP and cGMP for the secretion of renin
by hydrolysis of cAMP that occurs in response to various phosphodiesterase (PDE) isoforms.
Among these, PDE 3 may play a particular role since it is inhibited by cGMP. As shown by Chiu
and Reid, cGMP can stimulate renin release by decreasing cAMP breakdown via attenuated PDE
3-activity. Accordingly, inhibition of PDE 3 also augments the renin secretory response to -
adrenoceptor stimulation. Friis and colleagues very recently employed an elegant technique to
further test the concept that cGMP enhances renin release through the blunting of cAMP
degradation. Two PDE 3 subtypes (A and B) have been suggested to mediate cross-talk between
cAMP and cGMP pathways in JGCs. The PDE 3 enzymes are specific for cAMP and, as
mentioned above, they are inhibited by cGMP. In the study by Friis et al., patch clamp
experiments were made on isolated JGCs. Increases in membrane capacitance indicate cell
surface area increase, and this is an accepted measure of exocytosis at the level of the single cell.
cGMP had similar effects on membrane capacitance to cAMP, although 10-fold higher
concentrations were required. This effect of cGMP on membrane capacitance was inhibited by
blocking PKA, thus underscoring that the cAMP-PKA pathway takes part in cGMP-mediated
responses of JGCs. Therefore renin release from JGCs is significantly regulated by degradation
of cAMP, which is modulated by cGMP inhibition of PDEs.

There is also a potent pressure-sensitive mechanism for renin release; its stimulation is
associated with activation of the sympathetic nervous system and release of hormones, such as
oxytocin, which stimulate renin release in rats via a -adrenergic receptor-dependent mechanism.

As mentioned before, the release of active renin from JGCs is considered to be the main rate-
limiting step in providing circulating renin. Remarkably, the stimuli that inhibit renin secretion,
e.g. increased arterial pressure or Ang II, increase intracellular free calcium. This is in contrast to
the other secretory cells of the organism, in which augmented free calcium levels lead to
enhanced depletion of secretory granules. Thus, this unique feature of renin secretion is
commonly referred to as the calcium paradox. The reason for the opposite effect of calcium on
renin secretion can be found in the origin of the renin storage granules that appear to be modified
lysosomes.

The membrane potential of JGCs acts in concert with the various mechanisms controlling renin
secretion. Again, calcium seems to play an important role in this context. For instance, voltage-
dependent L-type calcium channels and calcium-sensitive voltage-gated calcium channels have
been identified in JGCs. The latter channels are sensitive to cAMP as they belong to the ZERO
variant, and play an important role in determining membrane potential. However, they are not
directly responsible for renin secretion, as their blockade does not affect renin secretion.
Conversely, activating the L-type calcium channels inhibits cAMP-mediated renin secretion, thus
providing evidence for a functional link between these channels and the control of renin
secretion.

Stages of kidney failure

BUN and Creatine on stages of kidney failure
Oliguria on Kidney disease