PowerPoint Presentation
GIT IN HEMODIALYSISBy: Ahmed EldeepMD
1
AGENDA 1- Common gastrointestinal (GI) symptoms among HD
patients.2-Abdominal pain in Dialysis patient.3- Are dialysis
patients at an increased risk of GI bleeding? 4-
Hemodialysis-associated ascites.
1
Common gastrointestinal (GI) symptoms
The CVS complications like hypotension & arrhythmia were at
the top with frequency of 79.3%. The GIT complications like nausea,
vomiting abdominal pain followed the CVS complication in decreasing
order of frequency. The other major proportion of complications was
Hematological complications
1-Nausea and vomitingOccurs in up to 10% of routine dialysis
treatments. Etiology The cause is multifactorial.Inadequate
dialysis. HypotensionEarly manifestation of disequilibrium
syndrome.Dialyzer reactions.Fluid and electrolyte changes during
the dialysis treatment.Non-dialysis causes(outside of the dialysis
setting) e.g: Hypercalcemia Cerebral causes or GI causes
Prior to the initiation of dialysis, patients may complain of
nausea and vomiting. These symptoms usually disappearwith dialysis
and removal of uremic toxins.
Etiology. Nausea or vomiting occurs in up to 10% of routine
dialysis treatments. The cause is multifactorial.Most episodes in
stable patients are probably related to hypotension. Nausea or
vomiting also can be an earlymanifestation of the so-called
disequilibrium syndrome described in II.A. Both type A and type B
varieties ofdialyzer reactions can cause nausea and vomiting.
Non-dialysis causes must always be considered when nauseaand
vomiting occur outside of the dialysis setting, as discussed in
Chapter 34. For example, hypercalcemia maymanifest as (primarily
interdialytic) nausea and vomiting, and should be looked for when
no other explanation is athand.2. Management. The first step is to
treat any associated hypotension. If nausea persists, an antiemetic
(seeTable 6-5) can be administered.3. Prevention. Avoidance of
hypotension during dialysis is of prime importance. In some
patients, reduction ofthe blood flow rate by 30% during the initial
hour of dialysis may be of benefit. However, the treatment time
mustthen be lengthened accordingly.6
Dyspepsia.
Dyspepsia. Dyspepsia is defined as persistent or recurrent
abdominal discomfort centered in the upper abdomen(epigastrium).
Dyspepsia and indigestion are terms that are frequently
interchangeable. Symptoms may includeepigastric pain or discomfort,
bloating, belching, eructations, and flatulence. Dyspepsia may be
due to a true GIpathologic process, such as peptic ulcer disease,
gastroesophageal reflux disease, gastritis, duodenitis,
orgastroparesis, as seen in diabetic patients. Alternatively,
dyspepsia may be related to medications that dialysispatients are
required to take, such as phosphate binders (e.g., calcium
carbonate or aluminum salts) or ironsupplements. Evaluation for
organic lesion is warranted if the history and physical examination
are suggestive of suchlesions. Prokinetic agents, antacids, and
histamine H2 receptor antagonists are the most widely used agents
in themanagement of dyspepsia. Dosing of these drugs in renal
failure is discussed below in Section II.A.3. (prokineticdrugs) and
Section II.B.3. (H2-blockers).7
2-Dyspepsia. Persistent or recurrent abdominal discomfort
centered in the upper abdomen epigastric pain or discomfort,
bloating, belching, eructations, and flatulence. EITIOLOGYTrue GI
pathologic process, such as peptic ulcer disease, GERD, gastritis,
duodenitis, or gastroparesis. Medications as phosphate binders
(e.g., calcium carbonate or aluminum salts) or iron supplements.
TTT: Prokinetic agents, antacids, and histamine H2 receptor
antagonists.
Dyspepsia. Dyspepsia is defined as persistent or recurrent
abdominal discomfort centered in the upper abdomen(epigastrium).
Dyspepsia and indigestion are terms that are frequently
interchangeable. Symptoms may includeepigastric pain or discomfort,
bloating, belching, eructations, and flatulence. Dyspepsia may be
due to a true GIpathologic process, such as peptic ulcer disease,
gastroesophageal reflux disease, gastritis, duodenitis,
orgastroparesis, as seen in diabetic patients. Alternatively,
dyspepsia may be related to medications that dialysispatients are
required to take, such as phosphate binders (e.g., calcium
carbonate or aluminum salts) or ironsupplements. Evaluation for
organic lesion is warranted if the history and physical examination
are suggestive of suchlesions. Prokinetic agents, antacids, and
histamine H2 receptor antagonists are the most widely used agents
in themanagement of dyspepsia. Dosing of these drugs in renal
failure is discussed below in Section II.A.3. (prokineticdrugs) and
Section II.B.3. (H2-blockers).8
3-Constipationcommon complaint among dialysis patients. The
causes of constipation are multifactorial. Patients' fluid intake
is limited. Dietary restriction of high-potassium fruits and
vegetables. Medications : calcium- or aluminum-containing phosphate
binders and iron supplements. Patient inactivity and underlying
medical conditions.
Constipation may result in obstruction, fecal impaction, and
even bowel perforation, diverticular disease, as well as
hemorrhoids.
Constipation. Constipation is not an uncommon complaint among
dialysis patients. The causes of constipationare multifactorial.
Patients' fluid intake is limited. Dietary restriction of
high-potassium fruits and vegetables decreasesthe fiber content of
ingested food. Medications such as calcium- or aluminum-containing
phosphate binders and ironsupplements cause constipation. Patient
inactivity and underlying medical conditions may contribute to
constipation.Narcotics given as an analgesic, such as codeine and
meperidine, can cause constipation, as well as mental statuschange
in patients with end-stage renal disease (ESRD).Constipation may
result in obstipation with obstruction, fecal impaction, and even
bowel perforation. Long-termcomplications of constipation are
thought to contribute to the etiologic process of diverticular
disease, as well ashemorrhoids. In patients treated with peritoneal
dialysis, decreased bowel motility can cause dialysate
outflowobstruction through the peritoneal catheter.9
Senna lax labImportal sachLactulose Laxel sachEnemax Picolax
drops
Management Increase the fiber content in food usually corrects
constipation. If constipation persists, the following agents may be
used: Emollient: docusate sodium (egycusate) 100 mg PO qd to tid ,
Stimulant: bisacodyl (Dulcolax) 13 tablets; and senna(senna lax lab
purgation).Hyperosmotic: sorbitol ( importal sach )70% 30 mL PO
qhs, lactulose 30 mL PO qhs. Sodium polystyrene sulfonate resin
plus sorbitol (Kayexalate) has been associated with intestinal
necrosis in ESRD patients, either given by enema or by the oral
route ( Dardik et al, 2000).
Dietary changes to increase the fiber content in food usually
corrects constipation. If constipation persists, thefollowing
agents may be used: Emollient: docusate sodium (Colace) 100 mg PO
qd to tid prn, casanthranol anddocusate sodium (Peri-Colace) 12
capsules or 12 tablespoons PO qhs prn; Stimulant: bisacodyl
(Dulcolax) 13tablets PO qd prn; and Hyperosmotic: sorbitol 70% 30
mL PO qhs, lactulose (Chronulac) 30 mL PO qhs. Sodiumpolystyrene
sulfonate resin plus sorbitol (Kayexalate) has been associated with
intestinal necrosis in ESRD patients,either given by enema or by
the oral route ( Dardik et al, 2000). It is not clear if the
sorbitol component alone is equallydangerous. Whereas the
combination is still widely used to treat hyperkalemia, use of
sorbitol to treat constipation,where there are alternatives
available, may not be wise. Soap suds, mineral oil, and tap water
enemas or bisacodyl orglycerin suppositories once daily may be used
for more immediate results. Colyte or GoLYTELY may be used forbowel
preparation for endoscopy or radiology studies despite the high
electrolyte content and the large volumeingested.Medicinal fiber in
the form of psyllium (Metamucil) should be avoided. Both sodium and
potassium are present in thepreparation, and a large volume of
liquid is required in preparation. Laxatives containing magnesium,
citrate, orphosphate should be avoided (e.g., milk of magnesium,
magnesium citrate, and Fleet's products containingphosphate).
Magnesium is poorly handled by patients with ESRD. Hypermagnesemia
can result in development ofneurologic disorders. Citrate, in
general, should be avoided in patients with ESRD because it
increases absorption ofaluminum from the GI tract.
Hyperphosphatemia from phosphate intake can upset the delicate
calcium/phosphorusbalance and contribute to the sequela of
secondary hyperparathyroidism.11
Medicinal fiber in the form of psyllium (Regmucil sach) should
be avoided. Both sodium and potassium are present in the
preparation. and a large volume of liquid is required in
preparation.Laxatives containing magnesium, citrate, or phosphate
should be avoided (e.g., milk of magnesium, magnesium citrate, and
Fleet's products containing phosphate). Magnesium is poorly handled
by patients with ESRD.
Hypermagnesemia can result in development of neurologic
disorders. (laxel sach- Epico-eff. Sach)Citrate, in general, should
be avoided in patients with ESRD because it increases absorption of
aluminum from the GI tract.(Mg citrate) Hyperphosphatemia from
phosphate intake can upset the delicate calcium/phosphorus balance
and contribute to the sequela of secondary
hyperparathyroidism.(Enemax- Laxel sach)Mg sulphate )Epsom salt-
laxel sach)Na picosulphate (picolax drops)
12
Senna lax labImportal sachLactulose Laxel sachEnemax Picolax
drops
4-DiarrheaAn episode of diarrhea.Diarrhea following a period of
constipation.An acute episode of bloody diarrhea associated with
abdominal pain, fever and signs of sepsis, and hypotension,
especially during hemodialysis, may suggest ischemic bowel disorder
or bowel infarction.Diarrhea associated with fever suggests an
infectious cause.
Persistent diarrhea requires a workup similar to that in
patients without ESRD. Suspect autonomic neuropathy in patients
with diabetes mellitus. Endoscopy is required to diagnose
inflammatory bowel disorders.
An episode of diarrhea on an occasional (bowel irritability
associated with dietary intake or viral GI disorder).Diarrhea
following a period of constipation may signal fecal impaction.
Treatment is focused on constipation.An acute episode of bloody
diarrhea associated with abdominal pain, fever and signs of sepsis,
and hypotension,especially during hemodialysis, may suggest
ischemic bowel disorder or bowel infarction.( ESRD patients are
prone to this disease because of their atherosclerosis-associated
risk factors such as hypertension, diabetes mellitus, and
Dyslipidemia).Diarrhea associated with fever suggests an infectious
cause. Blood and stool specimen for culture and sensitivity
arerequired. Clostridium difficile enteritis may occur after
prolonged antimicrobial therapy. Oral vancomycin ormetronidazole is
used in the treatment of C. difficile enteritis.
Persistent diarrhea requires a workup similar to that in
patients without ESRD. Suspect autonomic neuropathy inpatients with
diabetes mellitus. Endoscopy is required to diagnose inflammatory
bowel disorders.
In noninfectious diarrhea, loperamide hydrochloride (Imodium) or
diphenoxylate hydrochloride and atropine sulfate(Lomotil) may be
used for temporary relief.
14
2
Abdominal pain in Dialysis patient
Case81-year-old female on hemodialysis C/O: worsening of
abdominal pain of 2 days duration. The pain started as a dull ache
over the lower abdomen 2 months earlier, diffuse but especially
prominent over the lower quadrant, and was unrelieved by analgesic
medications. EX.: her whole abdomen was diffusely tender, but the
lower quadrant was extremely tender with palpable nodular lesions.
Lab: normal amylase and lipase level along with a white cell count
of 13.5K/CUMM (3.5- 10.6 K/CUMM), calcium of 10.6 mg/dL (8.2-10.6
mg/dL), phosphorus of 5.9 mg/dL (2.3-5.0 mg/dL) and intact PTH 880
pg/mL (18-86 pg/mL). CT abdomen and pelvis and ultrasound of her
abdomen revealed .
Causes of abdominal pain in dialysis patientGIT causes:Upper GI
diseases.Lower GI diseases.Hepato-biliary.Pancreatic.Non-GIT
causes:
Upper GI diseases: e.g., Gastritis, duodenitis, and peptic ulcer
disease.
Lower GI diseases:Diverticulosis and
diverticulitisConstipation.Colonic diverticula increased among pt
with polycystic kidney disease.B. Spontaneous colonic perforation.
diverticular disease, amyloidosis, constipation,
post-transplantation immunosuppressive treatment, and infections.C.
Discrete colonic ulceration.discrete, nonspecific single ulcers of
the cecum or ascending colon. D. Colonic carcinoma.
A. Diverticulosis and diverticulitis. Right-sided diverticular
disease is more common in the dialysis population thanin the
general population. Constipation due to dietary restriction of
fluid, fruits, and vegetables and due to the use ofcertain
phosphate binders predisposes dialysis patients to diverticular
disease. Colonic diverticula are increasedamong those suffering
from polycystic kidney disease. These large diverticula are prone
to perforate. Complicationsof diverticulosis include diverticulitis
and colonic perforation. Diverticulitis is a relative
contraindication for peritonealdialysis. In renal transplant
candidates with recurrent diverticulitis, segmental resection of
the lesions prior totransplantation may prevent subsequent
perforation when high-dose steroid therapy is initiated after
renaltransplantation.B. Spontaneous colonic perforation.
Spontaneous colonic perforation may be seen in patients with
increased risk,such as those with diverticular disease,
amyloidosis, constipation, post-transplantation immunosuppressive
treatment,and infections. Spontaneous perforation may occur in the
absence of an obvious cause or risk factor. A
vasculiticpathogenesis has been proposed. When a patient receiving
dialysis presents with abdominal pain, considerimpending or actual
colonic perforation. If perforation occurs, the mortality rate is
extremely high.C. Discrete colonic ulceration. A patient with ESRD
who is receiving hemodialysis and who presents withsymptoms similar
to those of appendicitis or carcinoma of the colon, or even with
rectal bleeding, may have discrete,nonspecific single ulcers of the
cecum or ascending colon. The pathogenesis of such lesions is
unknown. Treatmentis oriented towards symptoms.D. Intestinal
necrosis. Necrosis of the small and large intestines has been
reported in renal failure patientsreceiving oral or rectal sodium
polystyrene sulfonate in sorbitol. Whether the culprit is the
exchange resin or sorbitolis under investigation.E. Colonic
carcinoma. With regard to colonic carcinoma, vigilance should be
exercised in their detection. At aminimum, the official clinical
practice guidelines for their detection in the general population
should also apply toESRD patients.20
Hepato-biliary.Chronic cholecystitis and cholelithiasis are
common in dialysis patients. Symptomatic patients can be treated
with laparoscopic cholecystectomy or traditional cholecystectomy.
Asymptomatic patients usually undergo cholecystectomy if they are
renal transplant candidates.
Pancreatic.Diagnosis in patients with renal failure is
confounded by the observation that serum concentrations of
pancreatic amylase and lipase are elevated in patients with ESRD in
the absence of acute pancreatitis.The highest levels of amylase and
lipase are noted in hemodialysis patients. The absolute values do
not exceed three times the upper limit of normal. The degree of
elevation is roughly proportional to the degree of renal
dysfunction.
Elevated baseline levels of serum amylase. In most dialysis
patients, due to the loss of urinary excretion,serum total amylase
activity is elevated up to three times the upper limit of normal,
even in the absence of clinicalevidence of pancreatitis. The
magnitude of elevation is higher in patients with acute renal
failure than in chronicdialysis patients. Serum amylase levels may
be spuriously low in peritoneal dialysis patients
usingicodextrin-containing dialysis solutions ( Schonicke et al,
1999). Serum concentrations of the pancreas-specific P3isoenzyme
have been variably reported to be increased or normal in
asymptomatic dialysis patients. In fact, P 3values exceeding three
times the upper limit of normal are seen in up to 18% of
asymptomatic dialysis patients. Incontrast, in the nonuremic
population, the P 3 amylase fraction is consistently absent and
appears only with acutepancreatitis.2. Question of occult
pancreatitis in dialysis patients. Autopsy studies of largely
asymptomatic dialysispatients have revealed a high incidence of
pancreatic abnormalities, including chronic pancreatitis. The
extent towhich persistent elevations of the serum amylase levels
are due to decreased catabolism of the enzyme versuspancreatitis is
not known.3. Serum and peritoneal fluid amylase levels during
pancreatitis in dialysis patients. In a dialysis patientsuspected
of having pancreatitis, the finding of a serum total amylase value
in excess of three times the upper limitof normal suggests that
pancreatitis is present. Unfortunately, very severe pancreatitis
can be present in dialysispatients with only slight, and therefore
nondiagnostic, elevations in the serum total amylase level. We have
foundelevation of the plasma P3 isoenzyme level to be a reliable
indicator of pancreatitis in dialysis patients ( Vaziri et
al,1988).The peritoneal fluid amylase concentration, easily
obtainable in patients receiving peritoneal dialysis, is not
asensitive indicator of pancreatitis because the peritoneal fluid
amylase levels can be only slightly elevated in thepresence of
severe pancreatitis. Nevertheless, an effluent amylase level
greater than 100 units per dL issuggestive of pancreatitis or some
other intra-abdominal catastrophe ( Caruana et al, 1987; Gupta et
al, 1992).B. Lipase1. Elevated baseline serum lipase levels in
dialysis patients. Serum lipase activity is elevated (as high
astwice the upper limit of normal) in about 50% of dialysis
patients. Serum lipase activity rises following hemodialysisdue to
(a) heparin-induced increase in lipolytic activity and (b)
presumably, ultrafiltration-inducedhemoconcentration. Therefore,
predialysis samples should be used for this test.C. Serum22
Non-GIT causes:Metabolic disorder, e.g. hyperlipidemia,
porphyria,calciphylaxix.Hematologic disorder, e.g., sickle cell
crisis, hemolysis, acute leukemia.Cardio/pulm. disorder, e.g.,
acute MI, pulmonary embolus, pneumonia, pericarditis.Endocrine
disorder, e.g., DKA, pheo, Addisons disease,
hyperparathyroidism.Neurologic, e.g., herpes zoster.Toxic, e.g.,
Drugs, toxins, narcotic withdrawal. Also, heat stroke.
Case81-year-old female on hemodialysis C/O: worsening of
abdominal pain of 2 days duration. The pain started as a dull ache
over the lower abdomen 2 months earlier, diffuse but especially
prominent over the lower quadrant, and was unrelieved by analgesic
medications. EX.: her whole abdomen was diffusely tender, but the
lower quadrant was extremely tender with palpable nodular lesions.
Lab: normal amylase and lipase level along with a white cell count
of 13.5K/CUMM (3.5- 10.6 K/CUMM), calcium of 10.6 mg/dL (8.2-10.6
mg/dL), phosphorus of 5.9 mg/dL (2.3-5.0 mg/dL) and intact PTH 880
pg/mL (18-86 pg/mL). CT abdomen and pelvis and ultrasound of her
abdomen revealed .
CT abdomen and pelvis without contrast showing multiple soft
tissue densities in the anterior abdominal wall (A). Calcification
of blood vessels within the abdomen and pelvis was also noted
(B).
Ultrasound of abdomen revealing subcutaneous nodule.
Both these findings in the setting of end stage renal disease
were consistent with calciphylaxis, a rare, and often fatal,
complication. Although ulceration is considered a hallmark of
calciphylaxis, it can also present as non-ulcerative nodular
lesions, as in our patient. (Fine et al.,2002).
With the above treatment, she had significant improvement of
symptoms. Our case highlights the need for emergency physicians to
be cognizant of this life-threatening complication in end stage
renal disease patients and of the fact that calciphylaxis has
different modes of presentation, among which is acute abdominal
pain. 27
3
Are dialysis patients at an increased risk of GI bleeding?
Upper GI bleeding
Etiology Angiodysplasia of the stomach or duodenum (24%),
Erosive gastritis (18%), Duodenal ulcer (17%), Erosive esophagitis
(17%),Gastric ulcer (12%), MalloryWeiss (8%), and Erosive
duodenitis (3%).Zuckerman et al (1985),
1. Incidence and etiology. According to one study, the sources
of upper GI bleeding are gastritis (38%),duodenal ulcer (24%),
duodenitis (14%), gastric ulcer (9.5%), esophageal varices (9.5%),
and MalloryWeiss tear(5%). Proposed mechanisms for upper GI
hemorrhage with chronic renal failure include disturbances in
serumgastrin, in gastric acid secretion, in the mucosal barrier,
and in the clotting process; the use of ulcerogenic drugs,such as
anti-inflammatory drugs that inhibit prostaglandin synthesis
(nonsteroidal anti-inflammatory drugs, orNSAIDs, and aspirin); and
infection associated with H. pylori.However, in another study by
Zuckerman et al (1985), angiodysplasia was the most common source
of upper GIbleeding, as well as recurrent bleeding in the patients
with renal failure. Causes for upper GI bleeding in patientswith
chronic renal failure are as follows: angiodysplasia of the stomach
or duodenum (24%), erosive gastritis(18%), duodenal ulcer (17%),
erosive esophagitis (17%), gastric ulcer (12%), MalloryWeiss (8%),
and erosiveduodenitis (3%). It is possible that angiodysplastic
lesions in both the upper and lower tract in these patients areno
more common than in the general population. However, they are
discovered more frequently because of theirgreater tendency to
bleed. It has been suggested that renal failure plays a role in the
pathogenesis of theselesions. One theory states that functional
failure of the precapillary sphincter due to volume overload
andsubmucosal venous obstruction leads to vascular ectasia. Another
theory states that a low blood flow state duringdialysis followed
by reactive hyperemia results in eventual angiodysplasia. Finally,
others suggest that potassiumor gastrin, agents known to reduce
precapillary arteriolar tone, have a causative role in the
development of theselesions. Angiodysplastic lesions in patients
with chronic renal failure are more likely to bleed30
upper GI (n=34), lower GI (n=14), and unknown (n=4).
Duodenal ulcer (26%) and gastric antral vascular ectasia (26%),
followed by gastric ulcer (14%).
*lower GI: colorectal cancer, angiodysplasia and ischemic
enteritis were identified in equal numbers (21%).
upper GI (n=34), lower GI (n=14), and unknown (n=4). Duodenal
ulcer (26%)and gastric antral vascular ectasia (26%) were the most
frequently identified causesof upper GI bleeding, followed by
gastric ulcer (14%). In patients with lower GIbleeding, colorectal
cancer, angiodysplasia and ischemic enteritis were identified
inequal numbers (21%).31
The aim of this study was to examine the risk of UGIB among the
dialysis patients during a 6-year period following their initiation
of hemodialysis (HD) therapy in Taiwan- a country with the highest
incidence of ESRD in the world, using general population as an
external comparison group.
The incidence rate of UGIB (42.01 per 1000 person-year) was
significantly higher in the HD cohort than inthe control cohort
(27.39 per 1000 person-years). After adjusting for potential
confounders, the adjusted hazardratios for UGIB during the 6-year
follow-up periods for HD patients was 1.27 (95% CI=1.03-1.57)
compared topatients in the comparison cohort.33
Proposed mechanisms for UGI Hge. with CRF include disturbances
in :Serum gastrin, in Gastric acid secretion, Mucosal barrier,
Clotting process,Use of ulcerogenic drugs(NSAIDs, and aspirin); and
Infection associated with H. pylori.
Diagnosis. Esophagogastroduodenoscopy (EGD)
Management. As nonuremic patients. ( nasogastric aspiration,
transfusion, H2 blockers or pump inhibitor and antacids).H2
blockers include Cemetidine ,ranitidine , famotidine, and
nizatidine . All of these drugs are partially excreted renally, and
their usual dosage should be reduced by at least 50% in CRF. For
nizatidine, the recommendation is to give 150 mg every other day
(versus the usual 150 mg twice a day dosing in nonuremic
patients).Proton pump inhibitor - Dosing is unchanged in renal
insufficiency.
35
Conclusions: Use of PPIs in patients dialyzed using a dialysate
[Mg] of 0.75-1.0 mEq/l is associated with hypomagnesemia. We
suggest monitoring plasma [Mg] in patients taking PPIs, with
discontinuation of the medication if possible and/or adjustment of
dialysate [Mg] to normalize plasma [Mg].
Serum magnesium levels are lower in PPI use. In the inammatory
statelow serum magnesium level is a signicant predictor of
mortality in hemodialysis patients.
AbstractIntroduction This study aimed to evaluate the
association between proton pump inhibitor (PPI)use and serum
magnesium levels, and the role of hypomagnesemia and PPI use as a
risk factor formortality in hemodialysis patients. Methods An
observational study, including a cross-sectionaland 1-year
retrospective cohort study. The study comprised 399 hemodialysis
patients at a singlecenter, and was conducted from January to
September 2014. Multiple linear regression analysiswas used to
investigate the independent relationship between serum magnesium
levels and base-line demographic and clinical variables, including
PPI and histamine-2 receptor antagonist use. Coxregression model
was used to identify lower serum magnesium level and PPI as a
predictor of1-year mortality. Findings Serum magnesium levels were
lower with PPI use than non-PPI use(2.39 6 0.36 vs. 2.56 6 0.39
mg/dL, P < 0.001). Multiple linear regression analysis showed
that PPIuse, low serum albumin levels, and low serum potassium and
high-sensitivity C-reactive protein(hs-CRP) levels were signicantly
associated with low serum magnesium levels. A total of 29deaths
occurred during the follow-up period. According to Cox regression
analysis stratied by hs-CRP, only high serum hs-CRP levels
(>4.04 mg/L) in association with low serum magnesium levelswas
an independent risk factor for 1-year mortality (hazard ratio:
2.92; 95% CI: 1.536.40,P < 0.001). Discussion Serum magnesium
levels are lower in PPI use. In the inammatory state, alow serum
magnesium level is a signicant predictor of mortality in
hemodialysis patients.
37
Antacids containing aluminum and magnesium hydroxide should be
avoided in dialysis patients to avoid aluminum toxicity and
hypermagnesemia. Sucralfate is a sulfated polysaccharide,,
complexed with aluminum hydroxide. Sucralfate should not be used in
dialysis patients because of the risk of intestinal aluminum
absorption ( Robertson et al, 1989 ).Risk factors for ulcer
formation (NSAIDs and aspirin ingestion, smoking, etc.) should be
eliminated if possible.
Angiodysplasia.
4
Hemodialysis-associated ascites
CaseA 53-year-old male, ESRD secondary to type2 DM on
maintenance HD for 2Y presented with ascites of six months
duration. He was on twice-weekly HD with target wt of 6870 kg,
which progressively reduced since the last two months. Examination:
BP: 130/80 mm Hg, he had moderate to massive ascites and no
palpable abdominal organomegaly. Investigations : Hb of 8.6 g/dL,
bl. urea of 84 mg/ dL, s cr. of 7.4 mg/dL, s. ca. of 8.7 mg/dL and
s. phosphorus of 3.9 mg/dL. His URR on dialysis was 56%.Ascitic
fluid analysis revealed an exudate with protein of 5.4 g/dL,
albumin of 2.3 g/dL, LDH of 145 U/L and cell count of 250, 95% of
which were lymphocytes. Serum albumin was low at 2.7 g/dL, with
SAAG of
