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PubMed2006

Chronic renal failure at the Olabisi Onabanjo University Teaching Hospital, Sagamu, Nigeria.

UNLABELLED: BACKGROUND AND OBJECTIVES OF THE STUDY: Chronic kidney disease is a common cause of morbidity and mortality in Nigeria. This study aims at determining the pattern of chronic renal failure (CRF) in a Nigerian University Teaching Hospital. METHODS: The study was a 10-year retrospective study of consecutive cases of CRF seen at Olabisi Onabanjo University Teaching Hospital, Sagamu, Ogun State, Nigeria. RESULTS: The frequency of CRF in the population was 3.6% (182 of 5,107). There were 90 males and 63 females (1.42:1). The peak age was between 20-49 years, with a mean of 39.6 +/- 14.8 (range 14-72 years). The commonest causes were chronic glomerulonephritis 63(41.2%), hypertensive nephrosclerosis 40(26.1%) and diabetes mellitus 20(13.1%). The commonest symptoms were oedema, vomiting, oliguria and dyspnea occurring at 118(77.1%), 96(62.7%), 89(58.2%) and 87(56.9%) respectively. The mean creatinine clearance value at presentation was 6.5 +/- 8.1 mls/min, while the commonest complications were hypertension 68 (44.4%), biventricular failure 32 (20.9%) and urinary tract infection 29 (19%). The mean presenting systolic and diastolic blood pressures were 167.34 +/- 37.6 mm Hg and 106.03 +/- 28.9 mmHg respectively. The mean total haemodialysis session per patient was 3.5 +/- 1.6 (range 1-7 sessions). Only 34(22.2%) of the patients were able to afford haemodialysis. The majority 21(61.8%) of these could only afford 3 haemodialysis sessions while only 2(5.9%) patients had up to 7 dialysis sessions in the center. CONCLUSION: Chronic glomerulonephritis, hypertensive nephrosclerosis and diabetes mellitus are the commonest causes of chronic renal failure in Nigeria. Most of the patients presented late. Cardiovascular complications and infections were responsible for a greater morbidity among the patients.

Adolescent↗

PubMed2000

Prostate elastosis: a microscopic feature useful for the diagnosis of postatrophic hyperplasia.

BACKGROUND: Elastosis of the prostate may be seen on needle biopsy and radical prostatectomy specimens, but its significance is unknown. Prostatic atrophy (or postatrophic hyperplasia) is one of the most frequent mimics of prostatic adenocarcinoma. OBJECTIVE: To observe the frequent occurrence of elastosis of the prostate stroma in areas of postatrophic hyperplasia. DESIGN: A step-section method was used to cut the posterior lobe (or peripheral zone) in coronal planes at intervals of 0.3 to 0.5 cm in 100 consecutive autopsy specimens of men older than 40 years. Elastosis was detected because of a basophilic tinge of the stroma on hematoxylin-eosin stain and confirmed using elastic fiber stains. Presence of elastosis correlated with the following variables: age, prostatic atrophy (simple, hyperplastic, or sclerotic), local arteriosclerosis, histologic carcinoma, high-grade prostatic intraepithelial neoplasia, benign or malignant nephrosclerosis, generalized atherosclerosis, nodular prostatic hyperplasia, and acute inflammation. For statistics, a stepwise linear regression method adjusted for age was used. RESULTS AND CONCLUSIONS: Elastosis was found in 65 of the prostates examined and was significantly more frequent with increasing age (P <.001), prostatic atrophy (P <.001), and local arteriosclerosis (P <.02). There was no significant relation to histologic carcinoma, high-grade prostatic intraepithelial neoplasia, benign or malignant nephrosclerosis, generalized atherosclerosis, nodular prostatic hyperplasia, and acute inflammation. The correlation with local arteriosclerosis favors a possible role of ischemia to its etiopathogenesis. The absence of correlation to neoplastic and preneoplastic lesions and the striking spatial relationship of elastosis to prostatic atrophy (or postatrophic hyperplasia) add a new microscopic feature for the diagnosis of this latter lesion, helping in the differential diagnosis with prostate adenocarcinoma.

Adult↗

PubMed2000

[The renin saga].

This saga is the story of a scientific development. From the search of a mechanism to explain high blood pressure, research was orientated to the functions of an omnipresent biochemical system. And from the search to elucidate the etiology of arterial hypertension, research has ended up studying the local, functional and structural activity of the renin-angiotensin system and the possibilities of interfering with its actions. Since Bright, left ventricular hypertrophy became associated with nephrosclerosis. Later on, clinical studies led Volhard and Fahr to associate nephrosclerosis to high blood pressure while biochemical research led Tigerstedt and Bergmann to demonstrate that renin was associated to high blood pressure. Two teams of investigators, one in Argentina and one in USA discovered the biochemical mechanism by which renin acted on arterioles and later on, two other teams, one in USA and one in England, discovered the biochemical steps leading to the synthesis of angiotensin II. Since Goldblatt's experimental design resulting in a reliable method to obtain arterial hypertension, more than 20 years had to elapse before renal artery stenosis became established as the main cause of clinical secondary arterial hypertension. The renin-angiotensin system became part of a very complex array of substances able to regulate local circulation directly or indirectly and angiotensin has become involved in the remodeling of the smooth muscles of arterioles and myocardium.

Animals↗

PubMed2003

Gastric angiodysplasia in patients undergoing maintenance dialysis.

We successfully used argon plasma coagulation (APC) to treat two cases of dialysis patients with hemorrhagic gastric angiodysplasia. Gastric angiodysplasia is recognized as an important cause of gastrointestinal bleeding. Angiodysplastic lesion confined to the gastric antrum was first described in 1953 and named gastric antral vascular ectasia (GAVE). The condition is characterized as submucosal capillary dilatation and fibromuscular hyperplasia. The typical finding of GAVE is the so-called watermelon stomach, attributable to vasodilatation. In case 1, a 69-year-old man was introduced continuous ambulatory peritoneal dialysis (CAPD) in July 1997 because of chronic renal failure due to nephrosclerosis. He was hospitalized for severe anemia in December 1997. Gastrointestinal fiberscopy (GIF) showed oozing in the antrum, and gastritis and esophagitis with sliding hernia. Famotidine was started and recombinant human erythropoietin (rHuEPO) was used for anemia. However, the severe anemia did not improve. The patient was hospitalized again for severe anemia and hematemesis. Another GIF showed typical watermelon stomach, which corresponded with GAVE. An APC was performed without complications. Three months later, the anemia was improved, and the dose of rHuEPO was reduced. In case 2, a 57-year-old woman was introduced to hemodialysis in 1998 for uremia due to nephrosclerosis. In October 2000, she was hospitalized for rHuEPO-resistant anemia. A GIF showed oozing in the antrum with diffuse vasodilation in the antrum; GAVE was diagnosed. An APC was carried out without complications. Three months later, anemia was improved. Recently, gastric angiodysplasia was reported to be an important complication in dialysis patients and was recognized as an important cause of rHuEPO-resistant anemia. Argon plasma coagulation is an effective treatment for gastric angiodysplasia in patients on dialysis.

Aged↗

PubMed1992

The pathological basis of chronic renal failure in Nigerians. An autopsy study.

With the aim of determining the relative prevalence of the diseases underlying chronic renal failure (CRF) in a large homogeneous black tropical population, the autopsy records of the Obafemi Awolowo University Teaching Hospital over a four year period were studied. Out of a total of 702 cases coming to autopsy during this period, 66 (9.4%) died as a result of CRF. The highest number of cases of CRF fell within the 31-40 year age group with a male/female ratio of 1.28:1. Chronic glomerulonephritis was responsible for 40.9% of cases, malignant nephrosclerosis 16.6%, benign nephrosclerosis 7.6% while endstage renal disease (ESRD) was responsible for 15.4%. A miscellaneous group of diseases was responsible for 19.7%, about half of which was due to chronic pyelonephritis. Rarer causes of CRF were diabetic nephropathy, multiple myeloma, systemic lupus erythematosus and analgesic nephropathy.

Adolescent↗

PubMed1991

Hypertension and the kidney.

Pathophysiologic and hereditary mechanisms impacting on the kidneys are crucial for the initiation and maintenance of essential hypertension. An appreciation of these renal mechanisms is important for the institution of appropriate antihypertensive therapy. The clinician must develop a physiologic algorithm to control systemic blood pressure while maintaining adequate blood supply to the kidneys. This approach is particularly important in patients at higher risk for progressive renal insufficiency (i.e., older patients, blacks, diabetics, and those with chronic renal failure). Better perfusion reduces the likelihood of activating the compensatory neurohormonal systems that augment the intrarenal effects of the renin-angiotensin-aldosterone and sympathetic nervous systems, which ultimately may be responsible for renal structural changes leading to nephrosclerosis. In addition, dietary concerns are also important, particularly in the patients with evidence of early renal disease. Controlling blood pressure in a physiologic way by using drugs that can potentially dampen neurohormonal systems may prevent or at least delay the development of nephrosclerosis. Thus, the clinician should use an individualized therapeutic approach to the patient with hypertension. If nonpharmacologic means of blood pressure control are unsuccessful, an attempt should be made to blend the specific physiologic needs of the patient with specified pharmacologic antihypertensive mechanisms, paying particular attention to the preservation of renal function and perfusion.

Clinical Protocols↗

PubMed1990

Hypertension with co-existing renal disease.

It is generally accepted that treatment of systemic hypertension protects the kidney from haemodynamically-mediated injury. However, renal function may deteriorate during traditional antihypertensive therapy. Currently, hypertensive nephrosclerosis accounts for approximately 26% of all end-stage renal disease (ESRD) in the United States. Furthermore, in spite of aggressive treatment of hypertension, there is no evidence of a reduction in the incidence of hypertensive nephrosclerosis as a cause of ESRD. A current hypothesis states that renal protection is dependent on control of systemic hypertension (when present), and control of glomerular hypertension (when present). Since angiotensin II is a potent vasoconstrictor of the postglomerular capillary bed, which increases glomerular capillary pressure, it is attractive to hypothesize that drug therapies which can interrupt the intrarenal generation of angiotensin II (ACE inhibitors), or drug therapies which may attenuate the intrarenal actions of angiotensin II (calcium antagonists), may be renal protective. ACE inhibitors do control both systemic and glomerular hypertension. Calcium antagonists do control systemic hypertension; they may control glomerular hypertension. Long-term clinical trials in hypertensive patients, comparing the renal effects of ACE inhibitors with other antihypertensive drug classes (including calcium antagonists), have not been reported. It remains to be determined if the potential differing effects of antihypertensive drug classes on the renal microcirculation do, or do not, translate into differing renal protective advantages to patients at risk for the development and/or progression of renal disease.

Angiotensin-Converting Enzyme Inhibitors↗

PubMedDate not supplied

Renal vascular lesions in systemic lupus erythematosus.

In the past, necrotizing vasculitis has been considered to be one of the dominant intrarenal vascular abnormalities in systemic lupus erythematosus (SLE). To test the validity of this statement, 70 consecutive renal biopsies from patients with SLE were reviewed. Light microscopy (LM) and immunofluorescence (IF) studies documented abnormalities, including thrombosis and nephrosclerosis, in 30 patients (43 percent), but no cellular infiltration of the vessel walls or other evidence of acute necrotizing vasculitis was seen. It is concluded that while intrarenal vasculopathy with thrombosis and nephrosclerosis is a common finding in SLE, our data and recently published studies suggest that acute necrotizing vasculitis occurs rarely, if at all, in SLE nephritis.

Humans↗

PubMed1989

[The pathogenesis of chronic renal failure].

The pathogenesis of terminal renal failure is discussed. The following are distinguished: 1. Renal failure occurring against a background of decompensated benign nephrosclerosis, primary and secondary malignant nephrosclerosis, and stenosis of the renal artery. 2. Renal failure caused by loss of glomeruli. It is pointed out that in most glomerulopathies, including diabetic glomerulopathy and renal amyloidosis, terminal renal failure only develops when accompanying disease of the postglomerular vessels leading to interstitial fibrosis impairs the outflow of blood from the glomerulus to such an extent that no more urine is produced. 3. Renal failure in disease of the tubules themselves. It is emphasized that acute renal failure only becomes chronic when interstitial fibrosis develops from the interstitial edema occurring in the early stage of the disease. 4. Renal failure occurring in primary diseases of the renal cortical interstitium. The chronic sclerosing renal diseases arising from acute interstitial nephritis are dealt with, as also are reflux nephropathy, incomplete obstructive nephropathy, analgesic nephropathy, and chronic interstitial rejection reactions in transplanted kidneys.

Amyloidosis↗

PubMedDate not supplied

[Angiographic and morphologic criteria of the manifestation of arteriolonephrosclerosis in vasorenal hypertension].

Parallel comparison of angiographic and morphologic indices of arterial nephrosclerosis levels was performed in 34 patients with vasorenal hypertension secondary to unilateral lesion of renal arteries. Coefficient of vascular picture absence zone in the kidney (30) presenting a percentage ratio of a vascular zone of kidney cortical layer and the total area of its section was employed. Amount of vascular index (ratio between the wall density of afferent glomerular arteriole and its lumen diameter) was used to assess arteriolosclerosis in morphologic examination of renal biopsy specimens. High level of reliable coefficient 30 in the evaluation of arteriolar nephrosclerosis degree was substantiated morphologically. Critical level of coefficient 30 was stated for the affected and contralateral kidneys, and its increase was suggestive of irreversible sclerosis of renal microvascular bed.

Adult↗

PubMed1989

Effect of camostat mesilate on heavy proteinuria in various nephropathies.

Camostat mesilate, a developed derivative of gabexate mesilate for oral use, was administered in a daily dose of 600 mg for 4 weeks to 17 patients with heavy proteinuria due to various nephropathies. Five patients had glomerulonephritis (3 patients with IgA nephropathy, one each with membranoproliferative GN and membranous nephropathy) and 3 had systemic vasculitis. These patients had been treated with glucocorticoid, cyclophosphamide, anticoagulants, and dipyridamole. Five patients had diabetic nephropathy and had been treated with conventional therapy including angiotensin converting enzyme inhibitors. Two cases with benign nephrosclerosis, one with Alport syndrome, and the rest with end-stage renal failure of undetermined cause were also included in this study. Urinary protein decreased promptly within 2 weeks (from 5.2 +/- 0.7 to 3.5 +/- 0.5, mean +/- SE, p less than 0.005), and serum total protein and albumin levels increased significantly. Serum creatinine levels did not change. Decreases in urinary protein excretion of more than 50% were observed in five out of eight patients with glomerulonephritis or systemic vasculitis, two out of five with diabetic nephropathy, and one with chronic renal failure. However, urinary protein excretion values remained at the same level in two patients with benign nephrosclerosis and a patient with Alport syndrome. We suggest that camostat mesilate caused a change in glomerular capillary permeability for macromolecules through its inhibitory effects on the kallikrein-kinin system, complement system, coagulation system, and platelet function, which contributed to the treatment of the various nephropathies.

Administration, Oral↗

PubMed1987

Relationship between blood pressure level, renal histopathological lesions and plasma renin activity in fawn-hooded rats.

The fawn-hooded rat (FH rat) develops hypertension accompanied with focal and segmental glomerulosclerosis and proteinuria, resulting in premature death. In a first experiment the relationship between renal lesions and blood pressure at various ages was investigated. In a second experiment blood pressure was measured weekly from 10 to 38 weeks of age in a number of male FH rats, followed by examination of renal tissues at 40 weeks of age. Plasma renin activity (PRA) had also been determined in individual FH rats. FH rats aged 4.5 weeks had no renal morphological abnormalities. The severity of the glomerulosclerosis increased with age and showed a positive relationship with blood pressure. The scores of the proteinaceous tubular casts also increased with age and they, too, showed a positive correlation with blood pressure. The severity of glomerulosclerosis and proteinaceous casts at 40 weeks of age was related positively to the course of blood pressure throughout life. The final blood pressure level showed a positive correlation with final PRA values. Only FH rats with malignant nephrosclerosis had high PRA values. The renal glomerular and vascular lesions in the FH rat, most likely caused by the hypertension, progressively deteriorate to malignant nephrosclerosis. At that stage PRA values are increased and may be contributing to the development of renal vascular lesions and acceleration of the hypertension.

Aging↗

PubMed1995

Spectrum of hereditary renal disease in a kidney transplant population.

Re-evaluation of the underlying renal disease in 1000 consecutive kidney transplant patients revealed 129 cases of adult autosomal dominant polycystic kidney disease and 60 clear and seven suspected cases with other hereditary renal disorders. Twenty-four of 60 patients had cystic/dysplastic disease--10 of these classified as nephronophthisis, five as polycystic disease, and nine with the renal affection as part of a congenital malformation syndrome. Thirteen patients had Alport's syndrome, nine were diagnosed with tubulointerstitial nephritis, and six had an adult form of focal segmental glomerular sclerosis (FSGS). Two had changes classified as nephrosclerosis, but with an autosomal dominant mode of inheritance. Finnish type congenital nephrotic syndrome was present in two children and familial amyloidosis in two adults. Two patients had an unclassified disease. During follow-up, five patients with cystic/dysplastic disorders manifested liver disease. None of the patients with FSGS had recurrence and none of the Alport patients had anti-GBM disease. There were no other complications related to the renal condition. In conclusion, hereditary disorders are underestimated in regular registries of patients with end-stage renal failure. An adult form of FSGS and what seems to be a hereditary form of nephrosclerosis are among those that merit further study.

Adolescent↗

PubMed1994

A kidney biopsy is clearly mandatory to confirm the indication of plasma exchanges in adult haemolytic uraemic syndrome.

In case of haemolytic uraemic syndrome, it is not always possible to identify on a pure clinical basis the different kidney lesions responsible for the syndrome. We report a series of six cases without thrombotic microangiopathy, which emphasizes the need to perform a kidney biopsy as early as possible, so as to confirm the actual usefulness of plasma exchanges (PE) commonly carried out in emergency in every case of adult haemolytic uraemic syndrome. PATIENTS AND METHODS--Files of patients who were treated for haemolytic uraemic syndrome over the past 14 years were reviewed. Patients in whom thrombotic microangiopathy had been excluded by renal histology data were studied. Every patient was promptly treated with hypotensive drugs, so as to obtain blood pressure levels not exceeding 160-90 mmHg. Dialysis was performed in two patients. Daily PE with fresh frozen plasma were carried out in three patients as early as the first 24 hours after admission, and discontinued immediately after thrombotic microangiopathy could be excluded. RESULTS--All the patients met the usual criteria for diagnosis of haemolytic uraemic syndrome. Elevated liver enzymes were also found in the four cases of preeclampsia, consisting with diagnosis of severe HELLP syndrome. One case was associated with oestrogen therapy. Glomerular lesions were seen in four patients: slight endotheliosis in three cases of preeclampsia; marked lesions of IgA mesangial deposits in the patient who had been treated by contraceptive pill. Three patients had acute tubular necrosis and three had intense lesions of nephrosclerosis. Complete remission was obtained in every case of preeclampsia. Renal failure persisted in two cases (IgA glomerulopathy and one case of nephrosclerosis). DISCUSSION--The histological heterogeneity of haemolytic uraemic syndrome has been already well demonstrated. Typical lesions of thrombotic microangiopathy are usually classified into predominant glomerular lesions, pure arteriolar and mixed lesions. In other cases, thrombotic microangiopathy is not found: kidney lesions may be glomerular (endotheliosis, various subtypes of glomerulonephritis), tubular (acute tubular necrosis) or vascular (nephroangiosclerosis). In every aetiological circumstance, several different lesions may be found together. The usefulness of PE has been proved in thrombotic thrombocytopenic purpura, has been suggested in haemolytic uraemic syndrome and to a lesser extent in persistently severe HELLP syndrome. Unfortunately, none of these reports gave any information about kidney lesions responsible of acute renal failure. CONCLUSION--The haemolytic uraemic syndrome is a syndrome: thrombotic microangiopathy has to be proven when treatment by PE is planned, except in some severe clinical circumstances.

Adult↗

PubMed1993

[Treatment of hypertension in kidney diseases].

The authors review recent therapeutic procedures in arterial hypertension associated with renal disease. Treatment of hypertension is comprehensive, it comprises non-medicamentous procedures, pharmacotherapy and in some affections also interventional and surgical therapy. Effective reduction of the blood pressure to values < or = 140/90 mmHg unequivocally retards progression of renal disease, the development of nephrosclerosis and delays the development of renal insufficiency. In medicamentous treatment of nephrogenic hypertension a wide range of conventional antihypertensive drugs is used. Their selection and dosage must be adapted to the type of the basic renal disease and the reduction of renal functions. Recently the demand has been raised that the antihypertensive drugs used should possess in addition to the blood pressure lowering effect also an additive renoprotective effect ensuing above all from diminished intraglomerular hypertension and undesirable hyperfiltration, a changed permeability of capillary membranes due to reduction of microalbuminuria and proteinuria or restriction of proliferation procedures. These demands are met by the angiotensin I-converting enzyme (ACEI) inhibitor. If the correct dosage is used, ACEI are, due to their excellent antihypertensive action, absence of undesirable metabolic sequelae and significant renoprotective effect, drugs of the first line in nephrogenic hypertension. The authors use above all ACEI with a long-term effect, i.e. those without a SH group in the molecule. Very small doses (e.g. 2.5 mg Enalapril per day) reduce microalbuminuria and proteinuria and retard progression of nephrosclerosis also in nephropathies without systemic hypertension, e.g. in diabetic glomerulosclerosis. The renoprotective effect is manifested more markedly in initial stages of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗

PubMed1997

Renovascular hypertension may cause nephrotic range proteinuria and focal glomerulosclerosis in contralateral kidney.

Little attention has been paid to nephropathies and proteinuria in renovascular hypertension (RVH). Recently there has been a growing interest in the conditions induced by RVH. 10 cases of RVH were diagnosed by angiography and renin sampling from renal veins in the last 6 years in our hospital. The patients were all male and mean age was 64 +/- 8 (SD) years. Data were as follow: protein excretion was 3.8 +/- 2.2 g/day (> or = 3.5 g/day in 8 patients), sBP 202 +/- 24 mmHg, dBP 113 +/- 17 mmHg, serum renin concentration 64 +/- 45 pg/ml, and ipsilateral/contralateral renal vein renin ratio 3.3 +/- 1.0. RVH was treated by nephrectomy in 3 patients, percutaneous transluminal renal angioplasty (PTA) in 2, and angiotensin converting enzyme inhibitors (ACE-I) administration in 8. Biopsies were performed on contralateral kidney in 4 patients. Focal segmental glomerulosclerosis (FGS) was found in 3 patients, and nephrosclerosis in 1, whereas only nephrosclerosis was found in nephrectomized kidneys in all 3 patients. After nephrectomy, PTA and the treatment by ACE-I, not only blood pressure but also proteinuria was markedly reduced. These findings suggest that severe stenosis of the renal artery led to renal ischemia, which activated renin excretion, to cause glomerular hyperfiltration through vasoconstriction of the efferent arterioles in the contralateral kidney. FGS-like lesion thus induced appeared to have caused massive proteinuria.

Aged↗

PubMedDate not supplied

The kidney as a victim of essential hypertension.

Over the past decade the prevalence of end stage renal disease has risen progressively in industrialized societies. According to the data of renal disease Registries hypertensive nephrosclerosis appears to be a very important cause of progressive renal disease. However epidemiological data on the risk of hypertensive patients to develop renal failure offer contrasting results. In observational longitudinal studies a higher rate of decline in renal function is generally found in hypertensive compared to normotensive subjects. On the other hand, the inability of antihypertensive therapy to influence kidney destiny emerges from the large majority of interventional studies on mild-moderate hypertension in caucasian patients. At variance, the role of hypertension as etiologic factor seems to be sufficiently clear in African Americ: hypertension is more common, more severe and less easily to handle in a black patients. It is probable that the diagnosis of hypertensive nephrosclerosis is a confounding label laidon a heterogeneous group of diseases comprising a true hypertensive nephropathy (typical of black patients) along with occlusive or atheroembolic diseases common in aged caucasian patients. Our future efforts will have to be directed towards better identifying and properly classifying the various subgroup in order to optimize the treatment and prevent renal failure.

Aged↗

PubMed1983

N-acetyl-beta-glucosaminidase and beta 2-microglobulin. Their urinary excretion in patients with renal parenchymal disease.

The urinary excretion of N-acetyl-beta-glucosaminidase (NAG) and beta 2-microglobulin (beta 2M) was studied in 43 patients with various forms of renal parenchymal disease. Patients with membranous nephropathy, membranoproliferative glomerulonephritis, focal segmental glomerulosclerosis, obstructive pyelonephritis, nephrosclerosis, and minimal change nephropathy generally had urinary NAG and beta 2M levels more than 3 SDs above those seen in normal subjects. Patients with progressive renal disease averaged higher NAG and beta 2M urinary levels than those with the same renal lesion and stable function. Since elevated urinary levels of NAG and beta 2M suggest renal tubular injury or dysfunction, our observations suggest tubulointerstitial involvement in a wide variety of renal diseases.

Acetylglucosaminidase↗