Identification of Factors Associated With Acute Tubular Necrosis Following Kidney Transplant in Northern Mexico: Increased Risk With Cold Ischemia After 8 Hours.

AIM: To identify potential risk factors associated with the incidence of acute tubular necrosis (ATN) following kidney transplant in a sample of patients from northern Mexico. METHODS: Secondary analysis of data extracted from clinical files of patients who underwent a kidney transplant between 2000 and 2017 at Christus Muguerza Hospital in the city of Chihuahua. The final sample with complete data included 485 patients. ATN was diagnosed in 13.2% of patients using pathologic, clinical, and laboratory criteria. Adjusted odds ratio (ORs) with 95% CIs from multivariate binary logistic regression were used to identify predictors of ATN. RESULTS: Only 4 of 21 variables analyzed remained statistically significant in the final adjusted model. Cold and warm ischemia followed time-trend patterns with higher odds with longer ischemia times. For cold ischemia, compared with 0 to 240 minutes, ORs were 1.32 (95% CI, 0.49-3.51) for 241-480 minutes, 4.87 (95% CI, 2.29-10.3) for 481-960 minutes, and 10.0 (95% CI, 2.86-35.0) for > 960 minutes; for warm ischemia, compared with 40 to 59 minutes, these were 6.27 (95% CI, 1.95-20.8) for 60-70 minutes and 10.32 (95% CI, 1.95-54.4) for 71-110 minutes. Hypotension during surgery was associated with a higher chance of ATN (OR, 15.9; 95% CI, 4.97-50.9). When the recipients' age was 30 years or older, the probability also increased significantly (OR, 2.88; 95% CI, 1.09-7.57). The final model fitted well and explained 27% of the probability to develop ATN after a kidney transplant. CONCLUSION: Shortening the duration of ischemia and avoiding hypotension during surgery is essential to prevent ATN following a kidney transplant.

Preconditioning donor with a combination of tacrolimus and rapamacyn to decrease ischaemia-reperfusion injury in a rat syngenic kidney transplantation model.

Reperfusion injury remains one of the major problems in transplantation. Repair from ischaemic acute renal failure (ARF) involves stimulation of tubular epithelial cell proliferation. The aim of this exploratory study was to evaluate the effects of preconditioning donor animals with rapamycin and tacrolimus to prevent ischaemia-reperfusion (I/R) injury. Twelve hours before nephrectomy, the donor animals received immunosuppressive drugs. The animals were divided into four groups, as follows: group 1 control: no treatment; group 2: rapamycin (2 mg/kg); group 3 FK506 (0, 3 mg/kg); and group 4: FK506 (0, 3 mg/kg) plus rapamycin (2 mg/kg). The left kidney was removed and after 3 h of cold ischaemia, the graft was transplanted. Twenty-four hours after transplant, the kidney was recovered for histological analysis and cytokine expression. Preconditioning treatment with rapamycin or tacrolimus significantly reduced blood urea nitrogen and creatinine compared with control [blood urea nitrogen (BUN): P < 0·001 versus control and creatinine: P < 0·001 versus control]. A further decrease was observed when rapamycin was combined with tacrolimus. Acute tubular necrosis was decreased significantly in donors treated with immunosuppressants compared with the control group (P < 0·001 versus control). Moreover, the number of apoptotic nuclei in the control group was higher compared with the treated groups (P < 0·001 versus control). Surprisingly, only rapamycin preconditioning treatment increased anti-apoptotic Bcl2 levels (P < 0·001). Finally, inflammatory cytokines, such as tumour necrosis factor (TNF)-α and interleukin (IL)-6, showed lower levels in the graft of those animals that had been pretreated with rapamycin or tacrolimus. This exploratory study demonstrates that preconditioning donor animals with rapamycin or tacrolimus improves clinical outcomes and reduce necrosis and apoptosis in kidney I/R injury.

Ozone postconditioning in renal ischaemia-reperfusion model. Functional and morphological evidences.

BACKGROUND: Ischaemia-reperfusion is one of the main causes of kidney complications. The most frequent lesion is acute tubular necrosis. Ozone oxidative preconditioning exerts a modulatory effect of redox state of renal cells in models of ischaemia-reperfusion, by stimulating endogenous antioxidant mechanisms. Similar results have been obtained in more recent studies using ischaemic postconditioning. OBJECTIVES: To evaluate the effect of ozone oxidative postconditioning on renal function and morphology in an ischaemia-reperfusion rat model. METHODS: We used forty female Wistar rats weighing between 150g-200g randomly divided into 4 groups (negative control, positive control, oxygen and ozone). The groups: positive control, oxygen and ozone were subjected to 60 minutes of ischaemia and 10 days of reperfusion. During reperfusion, the oxygen group was given 26mg/kg body weight of oxygen, and the ozone group 0.5mg/kg body weight of ozone, rectally. At the end of the experiment urine and blood samples were taken for renal function tests and kidneys were removed for histological study. RESULTS: The ozone group showed no significant differences for filtration fraction and proteinuria compared to the negative control group. The glomerular filtrate rate, renal plasma flow and creatinine showed a slight improvement in comparison with oxygen and positive control groups. The ozone group showed significantly less overall histological damage than the positive control and oxygen groups. CONCLUSIONS: Ozone postconditioning showed to have a protective effect in preserving renal function and morphology.

Challenges in clinical-pathologic correlations: acute tubular necrosis in a patient with collapsing focal and segmental glomerulosclerosis mimicking rapidly progressive glomerulonephritis.

Herein, we report a case of acute kidney injury (AKI) due to diarrhea-induced acute tubular necrosis (ATN) in a patient with nephrotic syndrome secondary to biopsy-proven collapsing focal and segmental glomerulosclerosis (FSGS). The clinical picture mimicked rapidly progressive glomerulonephritis (RPGN) and motivated pulse therapy with methylprednisolone and cyclophosphamide. The case presentation is followed by a brief overview of the epidemiology of AKI in nephrotic syndrome as well as a discussion of its risk factors and potential mechanisms involved.

Effect of uric acid on gentamicin-induced nephrotoxicity in rats - role of matrix metalloproteinases 2 and 9.

In this work, we aimed to study the effect of uric acid on gentamicin-induced nephrotoxicity. Male Sprague-Dawley rats were assigned to one of six groups (six rats each) which received intraperitoneal injections for 9 days: (S) saline; (UA) Uric acid alone; (G) Gentamicin alone; (G + UA) Gentamicin + uric acid; (G rec) Gentamicin recovery and (G + UA rec) Gentamicin + uric acid recovery. In (G rec) and (G + UA rec), rats recovered for 7 days after the last injection. Urine and blood samples were taken on day 0 and at the end of every stage. Kidneys were harvested for histological scoring, determination of renal malondialdehyde (MDA), zymography and western blots for matrix metalloprotease (MMP)-2 and MMP-9. Uric acid alone did not provoke changes in biochemical and histological parameters when compared to controls. Gentamicin alone increased significantly plasma creatinine and blood urea nitrogen and caused a moderate histological damage. When combined with uric acid, these conditions worsened. MMP-9 activity and expression was decreased in rats from group G + UA as compared with rats from group G, while activity of MMP-2 was similarly increased in both groups when compared to controls. The increase in renal MDA induced by gentamicin was not altered when it was combined with uric acid. During the recovery stage, all biochemical parameters returned to normal levels, though a trend for delay of tubular damage recovery was observed in group G + UA rec when compared with group G rec. The results indicate that uric acid worsens gentamicin-induced nephrotoxicity. The mechanism is likely to implicate down-regulation of MMP-9.

Acute renal failure induced by carbon tetrachloride in rats with hepatic cirrhosis.

Relationship between cirrhosis and renal dysfunction is not yet fully understood. A model of cirrhosis with acute hepatic and renal damage (RF), produced by CCl4 in rats, with hemodynamic and renal functional alterations, similar to those observed in decompensated cirrhosis (DC) in man, was used to study chemical nephrotoxicity in animals. We performed in male Wistar rats hepatic and renal functional and hemodynamic studies in control, cirrhotic and decompensated cirrhotic (DC) groups. Cirrhosis was induced with carbon tetrachloride by chronic administration. Association between liver and renal functional alterations was detected in rats with decompensated cirrhosis, showing fall in mean arterial pressure and reduction of glomerular filtration rate and filtration fraction. Renal hemodynamics did not change in cirrhotic rats, similarly to what occurs in compensated cirrhotic patients. However, DC rats exhibited increased sodium, glucose and phosphate urinary excretions and decreased ATP in renal cortex. DC animals had severe hypoglycemia. There was an extensive liver fibrosis. Glomeruli had hypercellularity and tubules showed extensive vacuolization in cirrhotic and DC rats. The present study suggests that in this model, damage typical of acute tubular necrosis ensues in cirrhotic rats. We describe functional and morphological damage in liver and kidney in a model of cirrhosis that might predispose to the development of acute renal failure when an individual with hepatic damage is exposed in acute way to chemical toxicants.

Ocular lesions and experimental choline deficiency.

Previous studies have shown ocular haemorrhages in choline-deficient rats. The aim of this paper is to study further the relationship between ocular and renal lesions and biochemical alterations in rats fed a choline-deficient diet. Fifty one weanling male Wistar rats, were divided into two groups. Thirty one of them were fed a choline-deficient diet and the rest was fed a choline-supplemented diet ad libitum. Animals from both groups were killed between the fifth and the eighth day. Urea, creatinine and homocysteine concentrations in blood were determined. Eyes were used for light microscopy study; high resolution light microscopy and the study of the retina as "rétine a plat". Kidneys were studied by light microscopy. Choline-supplemented rats did not show ocular or renal lesion. Choline-deficient rats that showed renal lesions, tubular or cortical necrosis, did not always have ocular changes. There were no ocular changes in the only choline-deficient rat without renal lesion. The ocular changes consisted mainly in haemorrhage in both cameras and ciliary and vitreous bodies. Correlations between ocular and renal lesion (r = 0.72, p < 0.0001, CI 95%: 0.48-0.86); ocular lesion and creatinine (r = 0.86, p < 0.0001, Cl 95%: 0.72-0.93) and ocular lesion and urea (r = 0.70, p < 0.0001, Cl 95%: 0.44-0.85) were positive. Choline-deficiency induces ocular haemorrhagic lesions after the development of renal necrosis. The ocular pathology could be due to the immaturity of the ocular vasculature at this age. The hyaloid, choroid and retinal system are involved.

Ocular lesions and experimental choline deficiency

Previous studies have shown ocular haemorrhages in choline-deficient rats. The aim of this paper is to study further the relationship between ocular and renal lesions and biochemical alterations in rats fed a choline-deficient diet. Fifty one weanling male Wistar rats, were divided into two groups. Thirty one ofthem were fed a choline-deficient diet and the rest was fed a choline- supplemented diet ad libitum. Animalsfrom both groups were killed between the fifth and the eighth day. Urea, creatinine and homocysteine concentrations in blood were determined. Eyes were used for light microscopy study; high resolution lightmicroscopy and the study of the retina as “rétine a plat”. Kidneys were studied by light microscopy. Cholinesupplementedrats did not show ocular or renal lesion. Choline-deficient rats that showed renal lesions, tubular or cortical necrosis, did not always have ocular changes. There were no ocular changes in the only cholinedeficient rat without renal lesion. The ocular changes consisted mainly in haemorrhage in both cameras andciliary and vitreous bodies. Correlations between ocular and renal lesion (r=0.72, p<0.0001, CI 95%: 0.48-0.86); ocular lesion and creatinine (r=0.86, p<0.0001, CI 95%: 0.72-0.93) and ocular lesion and urea (r=0.70, p<0.0001, CI 95%: 0.44-0.85) were positive. Choline-deficiency induces ocular haemorrhagic lesions after the development of renal necrosis. The ocular pathology could be due to the immaturity of the ocular vasculature at this age. The hyaloid, choroid and retinal system are involved

Estudios previos han demostradohemorragia ocular en ratas deficientes en colina. El objetivo de este trabajo es profundizar en la relación entre las alteraciones oculares, renales y bioquímicas en ratas deficientes en colina. Cincuenta y una ratas Wistar macho recién destetadas fueron divididas en dos grupos: treinta y una fueron alimentadas con una dieta colino deficiente y el resto con colina suplementada ad-libitum. Los animales de ambos grupos fueron sacrificados entre el quinto y el octavo día. Se midió la concentración de urea, creatinina y homocisteína en sangre. Los ojos fueron estudiados por microscopía de luz, microscopía óptica de alta resolución y para el estudio de la retina como retina plana. Los riñones fueron estudiados por microscopía de luz. Las ratas suplementadas con colina no mostraron lesiones oculares o renales. Las colino deficientes que mostraron lesiones renales, necrosis tubular o cortical, no siempre tuvieron cambios oculares. No se encontraron cambios oculares en la única rata deficiente en colina sin lesión renal. Los cambios oculares consistieron principalmente en hemorragia enambas cámaras, cuerpo ciliar y vítreo. La correlación entre la lesión ocular y renal (r=0.72, p<0.0001, CI 95%:0.48-0.86), lesión ocular y creatinina (r=0.86, p<0.0001, CI 95%: 0.72-0.93) y lesión ocular y urea (r=0.70,p<0.0001, CI 95%: 0.44-0.85) fue positiva. La deficiencia de colina induce lesiones oculares luego del desarrollode la necrosis renal. La patología ocular podría ser debida a la inmadurez de los vasos oculares. El sistemahialoide, coroideo y retinal están involucrados

Ocular lesions and experimental choline deficiency

Previous studies have shown ocular haemorrhages in choline-deficient rats. The aim of this paper is to study further the relationship between ocular and renal lesions and biochemical alterations in rats fed a choline-deficient diet. Fifty one weanling male Wistar rats, were divided into two groups. Thirty one ofthem were fed a choline-deficient diet and the rest was fed a choline- supplemented diet ad libitum. Animalsfrom both groups were killed between the fifth and the eighth day. Urea, creatinine and homocysteine concentrations in blood were determined. Eyes were used for light microscopy study; high resolution lightmicroscopy and the study of the retina as ¶rétine a plat÷. Kidneys were studied by light microscopy. Cholinesupplementedrats did not show ocular or renal lesion. Choline-deficient rats that showed renal lesions, tubular or cortical necrosis, did not always have ocular changes. There were no ocular changes in the only cholinedeficient rat without renal lesion. The ocular changes consisted mainly in haemorrhage in both cameras andciliary and vitreous bodies. Correlations between ocular and renal lesion (r=0.72, p<0.0001, CI 95%: 0.48-0.86); ocular lesion and creatinine (r=0.86, p<0.0001, CI 95%: 0.72-0.93) and ocular lesion and urea (r=0.70, p<0.0001, CI 95%: 0.44-0.85) were positive. Choline-deficiency induces ocular haemorrhagic lesions after the development of renal necrosis. The ocular pathology could be due to the immaturity of the ocular vasculature at this age. The hyaloid, choroid and retinal system are involved (AU)

Estudios previos han demostradohemorragia ocular en ratas deficientes en colina. El objetivo de este trabajo es profundizar en la relación entre las alteraciones oculares, renales y bioquímicas en ratas deficientes en colina. Cincuenta y una ratas Wistar macho recién destetadas fueron divididas en dos grupos: treinta y una fueron alimentadas con una dieta colino deficiente y el resto con colina suplementada ad-libitum. Los animales de ambos grupos fueron sacrificados entre el quinto y el octavo día. Se midió la concentración de urea, creatinina y homocisteína en sangre. Los ojos fueron estudiados por microscopía de luz, microscopía óptica de alta resolución y para el estudio de la retina como retina plana. Los riñones fueron estudiados por microscopía de luz. Las ratas suplementadas con colina no mostraron lesiones oculares o renales. Las colino deficientes que mostraron lesiones renales, necrosis tubular o cortical, no siempre tuvieron cambios oculares. No se encontraron cambios oculares en la única rata deficiente en colina sin lesión renal. Los cambios oculares consistieron principalmente en hemorragia enambas cámaras, cuerpo ciliar y vítreo. La correlación entre la lesión ocular y renal (r=0.72, p<0.0001, CI 95%:0.48-0.86), lesión ocular y creatinina (r=0.86, p<0.0001, CI 95%: 0.72-0.93) y lesión ocular y urea (r=0.70,p<0.0001, CI 95%: 0.44-0.85) fue positiva. La deficiencia de colina induce lesiones oculares luego del desarrollode la necrosis renal. La patología ocular podría ser debida a la inmadurez de los vasos oculares. El sistemahialoide, coroideo y retinal están involucrados (AU)

Ocular lesions and experimental choline deficiency

Previous studies have shown ocular haemorrhages in choline-deficient rats. The aim of this paper is to study further the relationship between ocular and renal lesions and biochemical alterations in rats fed a choline-deficient diet. Fifty one weanling male Wistar rats, were divided into two groups. Thirty one ofthem were fed a choline-deficient diet and the rest was fed a choline- supplemented diet ad libitum. Animalsfrom both groups were killed between the fifth and the eighth day. Urea, creatinine and homocysteine concentrations in blood were determined. Eyes were used for light microscopy study; high resolution lightmicroscopy and the study of the retina as ¶rétine a plat÷. Kidneys were studied by light microscopy. Cholinesupplementedrats did not show ocular or renal lesion. Choline-deficient rats that showed renal lesions, tubular or cortical necrosis, did not always have ocular changes. There were no ocular changes in the only cholinedeficient rat without renal lesion. The ocular changes consisted mainly in haemorrhage in both cameras andciliary and vitreous bodies. Correlations between ocular and renal lesion (r=0.72, p<0.0001, CI 95%: 0.48-0.86); ocular lesion and creatinine (r=0.86, p<0.0001, CI 95%: 0.72-0.93) and ocular lesion and urea (r=0.70, p<0.0001, CI 95%: 0.44-0.85) were positive. Choline-deficiency induces ocular haemorrhagic lesions after the development of renal necrosis. The ocular pathology could be due to the immaturity of the ocular vasculature at this age. The hyaloid, choroid and retinal system are involved (AU)

Estudios previos han demostradohemorragia ocular en ratas deficientes en colina. El objetivo de este trabajo es profundizar en la relación entre las alteraciones oculares, renales y bioquímicas en ratas deficientes en colina. Cincuenta y una ratas Wistar macho recién destetadas fueron divididas en dos grupos: treinta y una fueron alimentadas con una dieta colino deficiente y el resto con colina suplementada ad-libitum. Los animales de ambos grupos fueron sacrificados entre el quinto y el octavo día. Se midió la concentración de urea, creatinina y homocisteína en sangre. Los ojos fueron estudiados por microscopía de luz, microscopía óptica de alta resolución y para el estudio de la retina como retina plana. Los riñones fueron estudiados por microscopía de luz. Las ratas suplementadas con colina no mostraron lesiones oculares o renales. Las colino deficientes que mostraron lesiones renales, necrosis tubular o cortical, no siempre tuvieron cambios oculares. No se encontraron cambios oculares en la única rata deficiente en colina sin lesión renal. Los cambios oculares consistieron principalmente en hemorragia enambas cámaras, cuerpo ciliar y vítreo. La correlación entre la lesión ocular y renal (r=0.72, p<0.0001, CI 95%:0.48-0.86), lesión ocular y creatinina (r=0.86, p<0.0001, CI 95%: 0.72-0.93) y lesión ocular y urea (r=0.70,p<0.0001, CI 95%: 0.44-0.85) fue positiva. La deficiencia de colina induce lesiones oculares luego del desarrollode la necrosis renal. La patología ocular podría ser debida a la inmadurez de los vasos oculares. El sistemahialoide, coroideo y retinal están involucrados (AU)

Renal involvement in human rabies: clinical manifestations and autopsy findings of nine cases from northeast of Brazil

Foi realizado estudo retrospectivo de nove casos de raiva internados em um hospital de Fortaleza, Brasil. Autópsia foi realizada em todos os casos. As idades variaram de 3 a 81 anos. Todos foram agredidos por cães. O tempo entre o acidente e a admissão hospitalar variou de 20 a 120 dias (média de 45 ± 34 dias). O tempo de internamento variou de 1 a 9 dias (média de 5.5 ± 3.1 dias). Os sinais e sintomas observados foram febre, hidrofobia, aerofobia, agitação, desorientação, dispnéia, sialorréia, vômitos, oligúria, faringite, dor e hipoestesia no local da mordida, cefaléia, síncope, tosse, hematêmese, midríase, hematúria, constipação, dor cervical e priapismo. Em três de seis pacientes (50%) foi encontrada evidência de insuficiência renal aguda, definida como creatinina > 1.4 mg/dL. Os achados de autópsia do tecido renal foram congestão glomerular leve a moderada e congestão capilar peritubular leve a intensa. Necrose tubular aguda foi encontrada em dois casos. Estes achados são inespecíficos, de modo que a instabilidade hemodinâmica, causada por disfunção autonômica, hidrofobia e desidratação podem ser considerados como responsáveis pela insuficiência renal aguda na raiva.

Renal involvement in human rabies: clinical manifestations and autopsy findings of nine cases from northeast of Brazil.

A retrospective study was conducted in nine patients with rabies admitted to a hospital of Fortaleza, Brazil. Autopsy was performed in all cases. The ages ranged from three to 81 years and six were males. They all were bitten by dogs. The time between the accident and the hospital admission ranged from 20 to 120 days (mean 45 +/- 34 days). The time until death ranged from one to nine days (mean 3.3 +/- 5.5 days). The signs and symptoms presented were fever, hydrophobia, aerophobia, agitation, disorientation, dyspnea, sialorrhea, vomiting, oliguria, sore throat, pain and hypoesthesia in the site of the bite, headache, syncope, cough, hematemesis, mydriasis, hematuria, constipation, cervical pain and priapism. In three out of six patients, there was evidence of acute renal failure, defined as serum creatinine > or = 1.4 mg/dL. The post-mortem findings in the kidneys were mild to moderate glomerular congestion and mild to intense peritubular capillary congestion. Acute tubular necrosis was seen in only two cases. This study shows some evidence of renal involvement in rabies. Histopathologic findings are nonspecific, so hemodynamic instability, caused by autonomic dysfunction, hydrophobia and dehydration must be responsible for acute renal failure in rabies.

Comprehensive surgical treatment of prune belly syndrome: 17 years' experience with 32 patients.

OBJECTIVES: To describe the results of comprehensive surgical management of prune belly syndrome. METHODS: Thirty-two patients were evaluated and treated for abdominal and genitourinary abnormalities. The surgical procedure, including simultaneous abdominoplasty, bilateral orchiopexy, and urinary tract reconstruction, was performed according to individual needs. At follow-up, the urinary tract, abdominal, and genital anatomy and function were evaluated. RESULTS: The upper urinary tract anatomy and function were stabilized in 30 patients, and no vesicoureteral reflux was found postoperatively. The bladder drainage was adequate in 29 patients, and 4 presented with recurrent bacteriuria. Abdominoplasty improved flaccidity in 29 patients. Adequate testicular position and consistency were obtained in 54 testes. Complications included acute tubular necrosis (1 patient) and ureterovesical obstruction (3 patients). CONCLUSIONS: Individualized comprehensive surgical management of prune belly syndrome is effective, with an acceptable incidence of complications and excellent long-term results.

Interstitial alterations in renal cortex in acute tubular necrosis (ATN) post-renal transplantation and in patients with ATN not related to renal transplant.

BACKGROUND: Abnormalities of renal function with long-term implications can persist after acute tubular necrosis (ATN), probably because of permanent loss of nephrons. Residual areas of fibrosis are also observed in the renal cortex post-ATN. In this study, we investigate the interstitial alterations post-ATN using histological and immunohistochemical methods. METHODS: We studied 11 patients with ATN of different etiologies and 19 patients with ATN post-renal transplantation. Eleven patients with ATN post-renal transplantation and one with ATN not related to renal transplantation were submitted to more than one biopsy because of delayed renal function recovery. The immunohistochemical studies were performed using alpha-smooth muscle-actin (alpha-SM-actin), endothelin, nuclear factor-kappaB (NF-kappaB), Jun-N-terminal kinase (p-JNK) and fibronectin antibodies. We also analyzed the urinary content of transforming growth factor-beta (TGF-beta) during the acute phase of ATN. RESULTS: The immunohistochemical studies showed increased alpha-SM-actin, fibronectin, endothelin, p-JNK and NF-kappaB staining in the tubulointerstitium area from the renal cortex of all patients when compared with controls (p < 0.001), and these increase persisted in the patients submitted to sequential biopsies. One of the patients with ATN without renal transplant and six patients with ATN post-renal transplant developed chronic renal failure. There was a significant increase of TGF-beta excretion in the urine of patients with acute renal failure (p < 0.01) compared with control. CONCLUSIONS: Our data show that the enhancement of renal TGF-beta production and the persistent increase of myofibroblasts, fibronectin, endothelin, p-JNK and NF-kappaB in renal cortex tubulointerstitium post-ATN may explain the impaired recovery of renal function observed in patients post-ATN frequently observed in patients with ATN post-renal transplant.

Pathology of renal diseases in the tropics

Renal diseases unique to the tropics are those that occur in association with infectious diseases including dengue hemorrhagic fever, typhoid fever, shigellosis, leptospirosis, lepromatous leprosy, malaria, opisthorchiasis, and schistosomiasis. These renal complications can be classified on the basis of their clinical and pathologic characteristics into acute transient reversible glomerulonephritis, chronic progressive irreversible glomerulonephritis, amyloidosis, and acute renal failure (ARF) resulting from acute tubular necrosis, acute tubulointerstitial nephritis, and thrombotic microangiopathy. Certain primary glomerular diseases including immunoglobulin (Ig) M nephropathy and focal segmental and global glomerulosclerosis are prevalent in some tropical countries. Renal complications of venomous snakebites also are common in the tropics. This article discusses and summarizes important works in the literature in respect to the clinical syndromes, pathologic features, and pathogenesis of tropical renal diseases both in humans and experimental animal models.

Trasplante renal: experiencia del Hospital Militar de Santiago / Renal transplant: experience at the Hospital Militar de Santiago

El trasplante renal es la mejor alternativa para el paciente insuficiente renal crónico, ya que logra una recuperación completa y queda libre de las limitantes de la diálisis crónica. El objetivo de este trabajo es presentar la experiencia en trasplante renal del Hospital Militar de Santiago. Para tal efecto, se realiza un estudio de cohorte histórico abierto de 153 trasplantes renales (TXR) realizados en 137 pacientes entre mayo de 1983 y mayo de 2002. Los pacientes fueron tratados con 4 esquemas de inmuno supresión: grupo1, prednisona + azatioprina (AZA) (n=15); grupo 2, prednisona + AZA + ciclosporina A (CsA) (n=85);grupo 3, prednisona + CsA+ inducción inmunoglubulina antitimocítica (ATG) (n=38); y grupo 4,prednisona + CsA + micofenolato mofetil (MMF) (n=15). La mediana de seguimiento fue de 48 meses (1-217). El 70,6 porciento de los TXR (108) fue de donante cadáver (DC) y el 29,4 porciento (45) fue con donante vivo (DV). La sobrevida actuarial global del injerto a 1, 2 y 10 años fue de 91,8 porciento, 86,7 porciento y 53,7 porciento, respectivamente. La sobrevida del injerto con DC es de 88,3 porciento al año y de 41,9 porciento a 10 años, siendo para el DV de 100 porciento y 75,9 porciento, respectivamente (p=0,0008). No hubo diferencias en la sobrevida del injerto si este fue riñón casa o del pool. En la serie, el 39,1 porciento de los trasplantados presentó necrosis tubular aguda (NTA), siendo un 6,6 porciento en DV y 52,8 porciento en DC (p<0,001). El tiempo de isquemia fría no influyó en una mayor incidencia de NTA. Rechazo agudo (RA), se observó en 53 pacientes (34,6 porciento), sin evidenciarse diferencias entre DV y DC. La histocompatibilidad no jugó ningún rol en el desarrollo de RA, como tampoco el tratamiento inmunosupresor. La causa más frecuente de pérdida del injerto fue el rechazo crónico (67,6 porciento). Treinta y tres pacientes presentaron algún tipo de complicación quirúrgica y de las complicaciones infecciosas, las más frecuentes fueron ITU, neumonía e infección por Citomegalovirus. De 19 pacientes fallecidos (12,4 porciento), las infecciones fueron su principal etiología. La sobrevida del injerto en nuestro grupo se compara con las series publicadas tanto nacionales como extranjeras, con muy buena sobrevida y morbilidad aceptable. Nuestra tasa de complicaciones quirúrgicas e infecciosas son similares a las reportadas por otros autores.

Complicaciones quirúrgicas en trasplante renal: experiencia Hospital Militar de Santiago / Surgical complications in kidney transplant: experience at the Hospital Militar de Santiago

La incidencia de complicaciones quirúrgicas (CQX) en el trasplante renal (TXR) fluctúa entre 3,7 y 15 porciento, causando ocasionalmente un deterioro de la función renal (FXR) o incluso la pérdida del injerto. El objetivo de este trabajo es presentar nuestra experiencia en las CQX, su impacto en la FXR y su relación con rechazo agudo (RA) y necrosis tubular aguda (NTA). Revisión retrospectiva de 153 trasplantes renales realizados entre mayo de 1983 y mayo de 2002 en el Hospital Militar de Santiago. Se evalúa la FXR durante la complicación y a largo plazo, y se estudia la relación entre RA o NTA (definida como la necesidad de diálisis) y la aparición de CQX. Con una mediana de 48 meses (1-217), identificamos 45 complicaciones en 33 pacientes, que incluyen 11 linfoceles (7,2 porciento), 7 hematomas perirrenales (4,6 porciento), 1 hemoperitoneo (0,6 porciento), 3 obstrucciones ureterales (1,9 porciento), 4 fístulas urinarias (2,6 porciento), 7 complicaciones vasculares (4,6 porciento) (2 trombosis arteriales, 4 estenosis arteriales y 1 trombosis venosa profunda) y 12 complicaciones de herida operatoria (7,8 porcientociones,4 hematomas, 1 dehiscencia y 1 seroma). El índice de CQX fue mayor en donante cadáver (20,1 porciento)que en donante vivo (11,1 porciento) (p=0,11). En los pacientes que sufrieron complicaciones, el promedio de tiempo en diálisis pretrasplante fue mayor que el de los que no se complicaron (25,9 m versus 18,8 m, p=0,09). El promedio de edad de los complicados fue mayor que el de los no complicados (43,2 versus 38,2 años, p= 0,09). No observamos una correlación significativa entre RA y CQX. Por otro lado, pacientes con NTA tuvieron un mayor índice de CQX (32 porciento versus 12 porciento, p= <0,05), específicamente para linfocele. La FXR se vio afectada durante la complicación en 14 de 33 pacientes (42,4 porciento), en 9 se recuperó a cortoplazo y en 5 de ellos, el riñón se perdió por esta causa. En el seguimiento de estos 33 pacientes complicados, 6 han fallecido, pero en ningún caso debido a la CQX. La edad pareciera ser un factor de riesgo de CQX. La complicación quirúrgica produce un deterioro de la función renal, que en la gran mayoría de los casos, se recupera a corto plazo. La necrosis tubular aguda influiría en una mayor incidencia de linfoceles.