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Anemia in KTR

Anemia can be defined as HB <12 g/dL in females & <13 g/dL in males, is commonly observed before and after KTx.

 

Anemia in KTR

 

Abbreviations (read twice please and put your comments):

o   +ve: Positive

o   AB: antibodies

o   ACEi: angiotensin-converting enzyme inhibitors

o   ALERT: Assessment of Lescol in Renal Transplantation study

o   APR: acute-phase reactant

o   ARBs: angiotensin receptor blockers

o   Aza: Azathioprine

o   BM: Bone marrow

o   BTx: blood (RBCs) transfusions

o    CAPRIT: Correction of Anemia and Progression of Renal Insufficiency in Transplant Patients

o   CHOIR: Correction of HB and Outcomes in Renal Insufficiency

o   CKD: Chronic kidney disease

o   CMV: cytomegalovirus

o   CNI: calcineurin inhibitors

o    CPGAABB: Clinical Practice Guidelines of the American Association of Blood Banks

o   CREATE: Cardiovascular Reduction Early Anemia Treatment Epoetin beta

o   CVD: Cardiovascular disease

o   CVS: Cardiovascular system

o   CyA: Cyclosporine

o   DCGS: death-censored graft survival

o   DGF: delayed graft function

o   Dgx: diagnosis

o   DX: Dialysis

o   EBV: Epstein-Barr virus

o   EC-MPS: enteric-coated mycophenolate sodium

o   eCrCl: Estimated creatinine clearance

o   eGFR: estimated glomerular filtration rate

o   EPO: erythropoietin

o    ESA: erythropoiesis-stimulating agent

o   ESKD: end-stage kidney disease

o   GI: gastrointestinal

o   HB: hemoglobin

o   HDX: hemodialysis

o   HF: heart failure

o   HUS: Hemolytic uremic syndrome

o   IF/TA: Interstitial fibrosis and tubular atrophy

o   IL-6: Interleukin-6

o    im/m: immunosuppressive/immunosuppression

o   IVIG: Intravenous immune globulin

o   KDIGO: Kidney Disease: Improving Global Outcomes

o   KTR: kidney transplant recipients

o   KTx: kidney transplantation

o   LDH: lactate dehydrogenase

o   LVH: Left ventricular hypertrophy

o   MAHA: microangiopathic hemolytic anemia.

o   MMF: Mycophenolate mofetil

o   MR: mortality

o   mTORi: mammalian (mechanistic) target of rapamycin inhibitors

o   NAAT: nucleic acid amplification testing

o   NICE: United Kingdom National Institute for Health and Care Excellence

o    NKF KDOQI: National Kidney Foundation Kidney Disease Outcomes Quality Initiative

o   NOA: new-onset anemia

o   PLS: Passenger leukocyte syndrome

o   Pph: plasmapheresis

o   Prox: prophylaxis/prophylactic

o   PVD: peripheral vascular disease

o   RBCs: Red blood cell

o   RCT: randomized controlled trial

o   RES: reticuloendothelial system

o   RETIC: Reticulocyte count

o   Rj: rejection

o   Sms: symptoms

o   Sns: signs

o   Snz: sensitization

o   SOT: Solid organ transplant

o   SRL: Sirolimus

o   Tac: Tacrolimus

o   TIBC: Total iron-binding capacity

o   TMA: thrombotic microangiopathy. 

o   TMP-SMX: Trimethoprim-sulfamethoxazole.

o   TR: transplant recipients

o   TREAT: Trial to Reduce Cardiovascular Events with Aranesp Therapy

o   TSAT: transferrin saturation

o   ttt: treatment

o   Tx: transplant

o   Tx: transplant/Transplantation

o   -ve: Negative

 

Anemia can be defined as HB <12 g/dL in females & <13 g/dL in males, is commonly observed before and after KTx. It’s mostly related to iron deficiency, graft Rj or dysfunction, EPO deficiency, viral infection, im/m, and infection Prox agents. We will discuss the epidemiology, pathogenesis, evaluation, and ttt of anemia in KTR. TR mostly have an average eGFR <60 mL/min/1.73 m2, a level that’s consistent with the current definition of CKD.







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 EPIDEMIOLOGY

The prevalence of anemia after KTx varies according to the given definition of anemia, the post-Tx timing, im/m protocol, and frequency of ttt. While anemia is found in almost 90 % of ptns within the 1st mo post-Tx, this prevalence declines to 34-45 % among ptns > one y. post-Tx. At the timing of Tx, most adult ptns can be termed anemic as target levels for HB among US DX ptns are mostly 10-11 g/dL. Mean HB levels rise to > 11 g/dL by 3 mo post-Tx and to > 12 g/dL at 6-12 mo post-Tx. The evolution of acute/chronic graft dysfunction is mostly associated with worsened anemia, e.g.:

o   At 6 mo post-Tx, about one-½ of ptns have an HB level below normal (defined as <14 g/dL in men & <12 g/dL in women).

o   At one y., 10-40 % are anemic despite showing normal graft function.

o   During the 1st 5-y post-Tx period, about one-1/3rd of ptns have HB <12 g/dL. More severe anemia, (HB <11 g/dL), seen in 12-15 % of ptns.

o   Registry study: 20 European centers, 3699 ped ptns Tx, 49.8 & 7.8 % of TR were anemic, according to the NKF KDOQI (defining anemia in children as HB < 5th percentile for age & sex) & NICE guidelines (defining anemia as HB <9.5 g/dL in ptns <2 ys old & <10 g/dL for ptns ≥2 ys old), resp. HB were strongly linked to allograft function. Low HB were correlated with higher risk of allograft failure or combined graft failure & death but not with death only.

PATHOGENESIS & RISK FACTORS

Pathogenesis of anemia after Tx varies by the timing after Tx. Common risk factors linked to anemia development may include female sex, age, graft dysfunction, ACEi/ARBs use, and im/m agents. Administration of ESA or iron therapy may be paradoxically associated with anemia owing to ttt via indication bias.

Early post-Tx: Immediate anemia after Tx is almost entirely due to lower-than-normal HB targets in the CKD & ESKD cohorts, surgical blood losses, and frequent phlebotomies. Dilutional anemia also occurs due to aggressive peri-operative volume expansion. Recovery to normal adult HB can be impeded by graft dysfunction and other comorbidities, higher donor age, and iron deficiency.

[1] Inadequate EPO: Improving erythropoiesis after KTx is due to the provided EPO from the graft and lack of the uremic milieu. Generally, EPO levels starts to rise on post-Tx day 2, reaching 4-folds at 2-3 weeks, after that time restored -ve feedback control ensue. Early EPO production can be inefficient in anemia correction as EPO seems still inefficient with the persisting uremic setting. Relative deficient EPO in the setting of graft dysfunction is mostly simulating that encountered with anemia in non-Tx-associated CKD. However, graft endocrine function may not be correlating with excretory function, mostly due to peri-tubular interstitial cells producing EPO, are selectively disabled or showed defective functional regulations. Anemia may be also corrected in some TR despite the relative lowered EPO levels.

[2] Iron deficiency: has a crucial role in persisting anemia in the immediate post-Tx period. Despite recognizing iron requirements for successful ESA therapy, iron deficiency still commonly encountered among ptns candidate for KTx. Iron stores may be seriously depleted after-Tx due to surgical blood losses, recurrent phlebotomy, and the utilized stores for triggered erythropoiesis. Return of normal menses with iron losses may be also contributing to iron deficiency in women.

The regulatory steps of iron absorption/mobilization from its stores to assist erythropoiesis is also disabled in the early post-Tx period and during Rj episodes. Hepcidin is the regulator of intestinal iron absorption & release of iron from RES stores. It is an APR, and its levels are increased in most DX ptns with poorly absorbed & mobilized iron for erythropoiesis. Hepcidin levels have also been found to be still elevated in many KTR, and the increased levels are correlated with poor Tx function, increased ferritin, and other inflammatory markers. IL-6, a crucial regulator of hepcidin production, has been shown to be increased immediately after Tx and within acute Rj episode.

The precise evaluation of iron stores after Tx is difficult as ferritin is a +ve APR while TSAT is varying inversely with APR. A higher ferritin level could be reflecting adequate iron storing, inflammation, or both, while low TSAT may be related to lowered iron stores, inflammation, or both. The combined [higher ferritin & low TSAT] is characterizing anemia of chronic disease and reflecting the impact of IL-6, hepcidin, and other inflammatory signals. Acute/chronic Rj, progressive drop in graft function, and inflammation or infectious episodes may induce ferritin rise. On the other hand, ferritin levels decline with iron consumption but also rising with enhanced GI iron absorption after Tx. So, ferritin levels are inconsistently reflecting iron stores among KTR and do not always reflecting anemia setting.  

[3] Donor kidney criteria: Cold/warm ischemic timing are not correlated with EPO levels. However, ptns with DGF have a slower production of EPO levels, which increases with improved allograft function. IF/TA in the donor kidney at timing of Tx have been shown to be associated with anemia at 12 mo after Tx.

Later (>3 mo) post-Tx

[1] im/m agents: The antimetabolites MMF, EC-MPS, & Aza can induce BM suppression, leading to anemia. However, the mean relative decline in HB level by these agents may only be 0.2-0.3 g/dL, resp. Generally, CNI do not induce BM suppression directly and do not typically induce anemia development. SRL also can also cause BM suppression and anemia, especially early after starting, but the effect could be lessened by time. Of note, SRL & the CNI (Tac & CyA) can also induce TMA-associated hemolytic anemia.  

[2] Other agents: Using ACEi/ARBs has been linked to anemia in a dose-related manner in KTR. According to this action, these agents have been also successfully used to control post-Tx erythrocytosis. Other agents commonly used in KTR causing anemia may include ganciclovir, valganciclovir, & TMP-SMX.

[3] Allograft dysfunction & Rj: In KTR, SCr levels >2 mg/dL (177 micromol/L) are tightly correlated with anemia. Moreover, episodic acute Rj also have been correlated with a medium decline of 0.5 g/dL in HB level that may be attributed to declined EPO production. Ptns returned to HDX after failed KTx are suffering from a chronic inflammatory status that’s complicated by resistance to ESAs action. Removal of the failed Tx in symptomatizing ptns can induce alleviation of the chronic inflammatory markers with recovered sensitivity to ESAs effects.

[4] Donor & recipient criteria: Donor of age >50-60 y. has been associated with a decline in EPO levels with increasing incidence of anemia. Women are more prone to develop post-Tx HB <12 g/dL at 6 & 12 mo. This may be due to the higher iron losses with menses as well as androgen level decline to men.

[5] Infections: Infections due to parvovirus B19, EBV, CMV, BK polyomavirus, varicella-zoster virus, TB, herpesviruses, & staph sp., have also been complicated with a greater risk of anemia.  

[6] Other causes: in the later post-Tx period may include certain comorbidities (new Dgx of HF, gastritis, PVD, & cerebrovascular events), secondary hyperparathyroidism, and folate/vit. B12 deficiency.

The PLS is a very rare syndrome for hemolytic anemia in SOT recipients that observed with ABO-compatible or Rh-compatible, but non-identical, donor and TR mismatching. PLS is most commonly reported after Tx of an organ from a donor with ABO-O blood type into a TR with ABO-A or -B blood type or from an Rh--ve donor into an Rh-+ve TR. The donor graft containing B cells & plasma cells (so-called passenger leukocytes) producing anti-isoagglutinin or anti-Rh AB leading to the syndrome development. PLS typically presented as a mild hemolytic anemia with an acute onset within the 1st few wks after Tx. Dgx can be made by the direct antiglobulin (Coombs) test. However, ttt is commonly supportive, despite Pph & cytolytic agents can be used. Clinical behavior is typically self-limiting, despite AB may be persisting at detectable values for 12-851 d.s after Tx.


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SCREENING: KTR should be currently screened for anemia after Tx via regular CBC. Most Tx centers obtain a CBC at least weekly for the 1st 3 mo and then every 2-4 weeks for a year and then monthly to every 3 monthly after that. Most TR are anemic at the timing of Tx and within the early post-Tx period, but HB levels are expected to gradually elevated along the 1st 3 mo post-Tx if the ptn has a well-functioned graft. So, the suggested approach to anemic ptns on routine screening:

o   Assessment of iron stores (S. iron, TIBC, % TSAT, S. ferritin).

o   TR < 3 mo post-Tx, no further testing unless ptns showed worsened anemia (i.e., HB decline to a level less than that at the timing of Tx).

o   Failed HB levels to be normalized by 3rd mo post-Tx > diagnostic assessment.

o   TR with HB levels normalized by 3 mo post-Tx, > diagnostic assessment for anemia if the ptn has developed NOA.

 

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DIAGNOSTIC ASSESSMENT:

KTR having persistent (i.e., HB fail to be normalized at 3 mo post-Tx) or NOA should proceed to diagnostic evaluation to recognize the etiology of anemia. This assessment should evaluate the cause(s) of anemia shared with non-Tx ptns, and other specific causes confined to KTR, via evaluating:

1)    History of blood losses

2)    Detailed dietary habits.

3)    RBCs indices & RETIC

4)    Testing for folate & vit. B12 deficiency

5)    Sms/Sns of infection (e.g., fever, malaise)

6)    Iron studies (S. iron, TIBC, % TSAT, S. ferritin)

7)    Graft function (SCr, spot urine protein-to-Cr ratio)

8)    Testing for presence of hemolysis (e.g., indirect bilirubin, LDH, haptoglobin)

9)    History for potential drug-induced anemia (e.g., MMF, EC-MPS, Aza, mTORi, ACEi, ARBs, ganciclovir, TMP-SMX

Routine evaluation of all anemic TR for infection with parvovirus B19 or other viruses is not performed. However, if the initial diagnostic assessment may not show a clear etiology for anemia, testing for parvovirus B19 can be proceeded via NAAT. Distinct evaluation of iron stores in KTR could be challenging. As lowered ferritin & TSAT means true deficiency, inflammation may suppress TSAT & elevate ferritin, masking the diagnostic value of these tests. Moreover, as no trials defining specified ferritin & TSAT levels for TR, criteria from the 2012 KDIGO Guideline for Anemia in CKD can be applied to determine iron deficiency. The concomitant finding of leukopenia, thrombocytopenia, and/or acute graft dysfunction are suggesting the following potential etiology for anemia:

o   Global myelosuppression, commonly induced by im/m, nutritional deficits, & Prox agents but can also be observed with viral infections.

o   HUS Dgx should be expected if anemia is seen with graft dysfunction, thrombocytopenia, and the finding of MAHA.

 

On contrary, parvovirus B19 infection or anti-EPO AB, expected with

1)    Lone anemia, (no leukopenia or thrombocytopenia)

2)    Lowered RETIC &

3)    No nutritional deficits.

 

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TREATMENT

General concepts: The general lines of anemia therapy in ptns with CKD or ESKD can be also applied to the ttt of anemia in KTR. These include ttt of the underlying cause(s) (if identified), ttt of iron deficiency, and the administration of ESA to decrease the need for RBCs transfusion. As applied in non-Tx ptns with CKD or ESKD, options of individual therapy relied mainly upon the severity of anemia and the finding of iron deficiency. Anemic ptns with iron deficits should be ttt with iron before commencing ESAs therapy.

Special considerations in ttt of anemia in KTR may include:

o   Target HB: Optimal target HB levels for KTR is not well determined and may vary according to allograft function.

o   Management of im/m & others: im/m agents, (EC-MPS, Aza, SRL) and other agents (e.g., ACEi/ARBs, ganciclovir, TMP-SMX) are current causes of post-Tx anemia. Dose decline/discontinuation of these agents may be indicated according to the timing from Tx and current status of the graft.  

o   Use of iron: It’s unknown whether IV or oral iron provides better ttt among KTR. With iron deficiency, we provide IV iron therapy rather than oral iron therapy. Several IV iron formulas are available, including ferric gluconate, iron sucrose, ferumoxytol, ferric carboxymaltose, & iron dextran. All of these formulas are equally effective, and selection may vary by team preference.

NB: oral iron has been inadequate to replace/maintain adequate iron stores and could bind with im/m members, e.g., MMF/MPS. Using PO4 binder ferric citrate that has been approved for ttt of iron deficits in CKD, has not been studied in KTR. Like standard oral iron agents, it can bind to im/m. Post-Tx erythrocytosis may develop in ptns on oral iron supplements. However, HB usually decline 4 weeks after iron withdrawal.

o   ESAs: Use of ESAs in KTR varies according to the timing from Tx, e.g., we do NOT provide ESAs immediately after Tx. With CKD anemia seen > 3 mo post-Tx in the iron-repleted ptn, we may provide an ESA. Ptns on ESA should be learned about the risk of stroke, thrombotic events, and possibly higher risk of recurrent cancer before commencing ESA therapy.

o   Using BTx: We should avoid using BTx if possible, to limit the risk of allo-Snz & Rj. However, if BTx is mandated in KTR, CMV-seronegative and/or filtered blood products are preferred to leukocyte-reduced products as CMV and other viruses can be transmitted in plasma. Blood products irradiation is not advised.

 

Approach based on timing from Tx: suggested approach to the ttt anemia in KTR varies mainly with the timing from Tx and the defined etiology of anemia.  

Ptns on waiting list: Anemia in ptns on waiting list should be ttt with the same approach applied in treat anemia in the CKD or ESKD cohort. Using RBC transfusion should be prohibited, if possible, to limit the risk of immunological Snz, that any delay or limit the option of future KTx. This’s consistent with the 2012 KDIGO guidelines for anemia ttt in ptns candidate for SOT.

Ptns perioperative/early post-Tx: Suggested approach is as follows:

o   Perioperative targeted HB of >10 g/dL that seems safe & limiting CVS events in the early post-Tx timing. The pre-Tx use of ESAs & iron in DX and pre-DX ptns should maintain HB between 10-11.5 g/dL, hence limiting peri-Tx RBC requirements. We limit RBC Tx to ptns with HB <7 g/dL or <8 g/dL in those with preexisting CVD that’s consistent with the 2016 CPGAABB.

o   With HB <10 g/dL and iron deficiency (i.e., TSAT20 % and S. ferritin ≤200 ng/mL) at the timing of Tx, we provide 1 g of IV iron (typically iron sucrose) with anticipated iron loss with phlebotomy during the early post-Tx timing. This’s based on a clinical experience and not based on high-quality evidence.

o   TR with previous ESA therapy, we often hold ESA at the timing of Tx as hypo-responsiveness to ESAs in the early post-Tx period, thrombotic & CVS risks of these agents, and the expected effect of endogenous EPO will ensue post-Tx. We do not provide ESAs to ptns with DGF, as using ESA agents in this population is debated and response to ESAs may be currently poor.

ESA agents immediately after-Tx may shorten the timing to correct HB but has not been proved to improve the clinical outcome. In RCT:104 ptns examining the effect of high-dosing EPO B before Tx and during the 1st 2 weeks after Tx, there was no difference in the rate of DGF between TR receiving and not receiving EPO. Also, a retrospective study: no difference in 3-mo HB values or DGF between TR receiving and not receiving EPO during the 1st 6 mo post-Tx.

2 studies: assessed the impact of high-dose EPO on DGF. One study: 72 ptns were assigned to get an intra-arterial EPO (40,000 units) or placebo at the timing of reperfusion of the graft. No difference seen between g.s in the need for DX within the 1st week or in the % of “slow graft function” (= 40 % decline in SCr by the 3rd day postoperatively). The 2nd trial: assigned 92 TR to IV EPO (33,000 units)/d./3 doses, starting 3-4 hs before Tx. EPO ttt had NO impact on the rate/duration of DGF but did augment the risk of thrombotic events at one mo. to one y.

Ptns later (>3 mo) post-Tx: Anemia in immediately post-Tx typically improved within 2-3 mo with endogenous EPO production from the graft. However, several factors, including im/m medications, others (e.g., ACEi/ARBs), graft dysfunction, and infection, may be contributing to persisting or NOA after the early post-Tx timing. Such potentially correctable factors should be recognized and ttt properly before starting ESA therapy. Moreover, the inlet to ttt of anemia in TR >3 mo post-Tx relied primarily upon the functional status of the renal allograft.

Ptns with stable allograft function: with stable allograft function (eGFR45 mL/min/1.73 m2), suggested approach may include:

o   Finding of folate and/or vit B12 deficits> correct the deficits.

o   Finding of iron deficiency, > ttt with IV iron.

o   With lack of definite cause of anemia & taking ACEi/ARBs, we balance the possible risks/benefits of keeping these agents. If the ptn has no urgent need to ACEi/ARBs to manage other comorbidities (e.g., HF), it’s reasonable to hold ACEi/ARBs. If anemia improved, ACEi/ARBs can be re-used later on (e.g., after one y), if indicated, with observing any worsened HB levels.

o   In ptns on high dosing of an antimetabolite (e.g., MMF 1000 mg twice/d. or EC-MPS 720 mg twice/d.) as maintenance im/m, we decrease the dosing, typically by 50 %, if anemia is severe and dose decrease is amenable, e.g., if the ptn is on EC-MPS 720 mg twice/d., we reduce to 360 mg twice/d. Also, if ptn is on MMF 1000 mg twice/d, we reduce the dose to 500 mg twice/d.

o   In ptns on ganciclovir and/or TMP-SMX, we assure that their proper dosing for the level of graft function. We do not reduce/hold these drugs to ttt anemia.

o   If anemia persists despite these regulations, we start an ESA with HB <9 g/dL & target HB of 10-11.5 g/dL that’re similarly advised for non-DX & DX CKD ptns. During routine monitoring, ptns may exceed 11 g/dL, the dose of ESA should be temporarily hold/reduced by 25 % monthly until reaching the target.

Optimum target HB level for TR with stable allograft function is not certain. Studies in KTR have suggested that MR may be triggered with HB >12.5 g/dL. However, one study has showed that allograft survival could be better among ptns with high HB level. The 2-y, open-label trial CAPRIT: 125 KTR with eCrCl <50 mL/min/1.73 m2 assigned ptns to get EPO targeting 13-15 g/dL (full correction g.) or 10.5-11.5 g/dL (partially corrected). Compared with the partially corrected g., complete correction g. had a little decline in eCrCl (5.9 vs 2.4 mL/min/1.73 m2), lowered rate of ESKD (21 vs 4.8 %), & higher DCGS (80 vs 95 %). This trial is limited by shortened duration, open-label design, and smaller size.

These findings are highly different from that reported by the much larger CHOIR & TREAT trials that randomly assigned non-Tx CKD ptns. The CHOIR & TREAT trials found a higher risk of CVS events and non-delay in progressive renal failure via normalizing HB by ESA agents. The CREATE trial applied anemia management like CAPRIT and showed that randomization to a higher HB level induced significant rise in chronic DX. It’s difficult to conclude the mechanism by which higher HB and/or more ESA may protect TR but not native one. Much larger trials comparing ESA with placebo are currently required to determine the risk/benefit ratio of anemia control among TR. Providing darbepoetin alfa is also often efficacious in KTR. Retrosp., 12-wk study: 36 ptns, 81 % achieving target HB of >12 g/dL (average 4.4 wks). A longer duration of ttt was needed with established anemia and/or exposing to concurrent ACEi agents.

 

Ptns with a failed allograftTR in stage 4/5 CKD usually became anemic, and ESA agents may be urgently provided to ameliorate Sms and limit the risk of BTx. Control of anemia in this population is simulating that in CKD/ESKD cohort, except that higher dosing of ESAs usually required to overcome the impact of chronic inflammation. Ptns with stable allograft function, any potential reversible cause should be addressed (e.g., nutritional deficits, iron deficiency, im/m, etc.). We start ESA therapy if HB between 9-10 g/dL and the iron stores seems adequate. We also evaluate the risks related to ESA agents that’re usually greater in ptn with CVD, previous thrombotic events, stroke, or prior cancer. With higher risks of ESA agents, we may avoid ESAs until the extent of anemia is more intense (i.e., HB <9 g/dL).  KTR returning to DX have lowered HB levels if compared with non-Tx CKD ptns (HB of 8.9 vs 10.2 g/dL, resp.) that correlated with higher hospitalization and increased MR. Using ESAs may decrease the frequency/intensity of anemia in ptns with failed Tx but have not been reported to decrease MR. Ptns returned to DX with ESAs resistance may benefit from graft nephrectomy.

Special populations: Ptns with parvovirus B19 infection: Anemia can be corrected by IVIG + decreasing im/m burden to enhance viral clearance.  

PROGNOSIS: debated findings have been reported regarding the prognosis of KTR with anemia. For better definition of this relation, the correlation between anemia (= <12 g/dL in females % <13 g/dL in males) and ptn allograft outcome was assessed in a prospective study: 938 KTR, at 4 ys, multivariate analysis showed that anemia was complicated with higher risk of MR & allograft failure. Similar findings were seen if anemia was defined = <11 g/dL. However, analyzing 825 KTR over 8.2 ys showed no relationship of anemia to MR.

In the ALERT study: 2102 KTR, 29 % of females & 30 % of males were anemic, HB were not complicated with any effect on CVS morbidity & MR or all-cause death after advanced adjustment for clinical & demographic factors. HB value, however, were passively associated with allograft loss. LVH, a crucial risk factor for CVS MR among CKD ptns, may be partially showing an impact of un-ttt anemia. As CVD is the leading cause of death in diabetic KTR, the adverse impacts of anemia may be clearer in diabetic KTR in the US, if compared with other countries, as the US Tx population has a relative increase in CVS risk, with a higher % in diabetics. Unfortunately, the current trials have not proved that robust ttt of anemia regresses /retards LVH progression, and any benefit of ESA use may be outweighed by their associated risks.

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Anemia in KTR
Anemia can be defined as HB <12 g/dL in females & <13 g/dL in males, is commonly observed before and after KTx.
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