Pattern Of Renal Injury Research Articles

MO196KIDNEY INVOLVEMENT IN WALDENSTROM MACROGLOBULINEMIA AND IGM MONOCLONAL GAMMOPATHY

Abstract Background and Aims Renal manifestations of IgM gammopathy are less common than those seen in patients with multiple myeloma. However, a wide spectrum of kidney diseases has been described in previous publications. We aim to characterize kidney involvement in patients with Waldenström Macroglobulinemia and IgM-secreting B cell lymphoproliferative disorders. Method We retrospectively studied 7 patients with a circulating monoclonal IgM and renal histology showing evidence of monoclonal immunoglobulin deposits or lymphomatous infiltration. Demographic, clinical and laboratory data were collected. Results Of the 7 patients studied, four (57%) were male and the median age was 68 years old (range 41-79). Among the 7 patients, 5 met criteria for Waldenström Macroglobulinemia after bone marrow biopsy; none of them had hyperviscosity syndrome. Four patients presented with nephrotic syndrome and all had impaired renal function and hypertension. Four patients had microscopic hematuria and only one patient showed no proteinuria. Mean serum creatinine levels were 2.9mg/dL. Renal biopsy showed different patterns of renal injury, including typical intracapillary monoclonal deposits disease (5 patients), membranoproliferative glomerulonephritis with cryoglobulinemia (1 patient), AL-amyloidosis (1 patient) and interstitial lymphoplasmacytic infiltration with CD20+ lymphocytes associated with minimal change disease. Follow-up data were obtained in 4 patients: 3 underwent chemotherapy but only one achieved complete remission and 2 progressed to end-stage renal disease. Conclusion Although rare, Waldenström Macroglobulinemia and IgM gammopathy are responsible for diverse manifestations of renal disease. A prompt diagnosis is of utmost importance in order to ensure early start of therapy, which should be directed at the underlying hematologic disorder, to improve renal survival.

Role of Oxidative Stress in Drug-Induced Kidney Injury.

The kidney plays a primary role in maintaining homeostasis and detoxification of numerous hydrophilic xenobiotics as well as endogenous compounds. Because the kidney is exposed to a larger proportion and higher concentration of drugs and toxins than other organs through the secretion of ionic drugs by tubular organic ion transporters across the luminal membranes of renal tubular epithelial cells, and through the reabsorption of filtered toxins into the lumen of the tubule, these cells are at greater risk for injury. In fact, drug-induced kidney injury is a serious problem in clinical practice and accounts for roughly 20% of cases of acute kidney injury (AKI) among hospitalized patients. Therefore, its early detection is becoming more important. Usually, drug-induced AKI consists of two patterns of renal injury: acute tubular necrosis (ATN) and acute interstitial nephritis (AIN). Whereas AIN develops from medications that incite an allergic reaction, ATN develops from direct toxicity on tubular epithelial cells. Among several cellular mechanisms underlying ATN, oxidative stress plays an important role in progression to ATN by activation of inflammatory response via proinflammatory cytokine release and inflammatory cell accumulation in tissues. This review provides an overview of drugs associated with AKI, the role of oxidative stress in drug-induced AKI, and a biomarker for drug-induced AKI focusing on oxidative stress.

Chronic Transplant Glomerulopathy-like Injury in Native Kidney After Allogeneic Bone Marrow Transplantation: A Possible New Pattern of Renal Injury Associated with Graft-vs-Host Disease

Chronic Transplant Glomerulopathy-like Injury in Native Kidney After Allogeneic Bone Marrow Transplantation: A Possible New Pattern of Renal Injury Associated with Graft-vs-Host Disease

Quadruple Nephropathy in a Liver Transplant Patient

Hepatitis C Virus (HCV) is associated with multiple renal diseases, namely cryoglobulinemic Membranoproliferative Glomerulonephritis (MPGN), IgA nephropathy, and diabetic nephropathy. The pattern of renal injury in patients with HCV-associated cryoglobulinemia is MPGN in nearly 80% of cases. The pathogenesis linking IgA nephropathy with HCV and cirrhosis remains unclear. HCV is associated with an increased risk of type 2 diabetes mellitus. Cirrhotic patients are at risk for Acute Tubular Necrosis (ATN) due to a tenuous hemodynamic state. We describe a case of quadruple nephropathy in a patient with HCV and diabetes mellitus who develops MPGN, IgA nephropathy, diabetic nephropathy and ATN.

Renal Trauma from Recreational Accidents Manifests Different Injury Patterns than Urban Renal Trauma

The majority of blunt renal trauma is a consequence of motor vehicle collisions and falls. Prior publications based on urban series have shown that significant renal injuries are almost always accompanied by gross hematuria alone or microscopic hematuria with concomitant hypotension. We present a series of blunt renal trauma sustained during recreational pursuits, and describe the mechanisms, injury patterns and management. Database review from 1996 to 2009 identified 145 renal injuries. Children younger than age 16 years, and trauma involving licensable motor vehicles, penetrating injuries and work related injuries were excluded from analysis. Grade, hematuria, hypotension, age, gender, laterality, mechanism, management, injury severity score and associated injuries were recorded. We identified 106 patients meeting the criteria and 85% of the injuries were snow sport related. Age range was 16 to 76 years and 92.5% of patients were male. There were 39 grade 1 injuries, 30 grade 2, 22 grade 3, 12 grade 4 and 3 grade 5 injuries. Gross hematuria was present in 56.7%, 77.2% and 83.3% of grade 2, grade 3 and grade 4 injuries, respectively. None of the patients with grade 2 or greater injuries and microscopic hematuria had hypotension except 1 grade 5 pedicle injury. The nephrectomy and renorrhaphy rate for grade 1 to grade 4 injuries was 0%. Compared to urban series of blunt renal trauma, recreationally acquired injuries appear to follow different patterns, including a paucity of associated injuries or hypotension. If imaging were limited to the presence of gross hematuria, or microscopic hematuria with hypotension, 23% of grade 2 to grade 4 injuries would be missed. Men are at higher risk than women. However, operative intervention is rarely helpful.

Mixed cryoglobulinaemia not related to hepatitis C virus, mesangiocapillary glomerulonephritis and lymphoplasmocytic lymphoma.

Kidney involvement associated to lymphoma is a known phenomenon but frequently not characterized due to the low frequency with which biopsies are realized in these patients. Several histological patterns can co-exist and happen unnoticed without a biopsy. Parenchyma infiltration in kidney for lymphoma has been found in 34% (post-mortem) and 14% (pre-mortem) and have low incident of clinical manifestations. Other patterns of renal injury are associated to lymphoma and minimal changes disease is especially related with Hodgkin's lymphoma. Renal lesions associated to paraprotein in lymphoplasmacytic lymphoma are an exceptional association, in spite of in 20% of them, appear cryoglobulinemia. There are a few cases reported in the literature with different histological patterns: light-chain disease, amyloidosis, and immunotactoid glomerulopathy related with kidney injury in patients with lymphoma. A 39-year-old male presented an association among paraproteinemia, membrano-proliferative glomerulonephritis no hepatitis C virus related and lymphoplasmacytic lymphoma with renal infiltration. This case emphasized the variety of renal lesions that lymphomas could trigger and the value of the nephropathology in the diagnosis and outcome of the hematologic diseases with paraproteinemia.

Urine Proteome Analysis May Allow Noninvasive Differential Diagnosis of Diabetic Nephropathy

OBJECTIVEChronic renal insufficiency and/or proteinuria in type 2 diabetes may stem from chronic renal diseases (CKD) other than classic diabetic nephropathy in more than one-third of patients. We interrogated urine proteomic profiles generated by surface-enhanced laser desorption/ionization-time of flight/mass spectrometry with the aim of isolating a set of biomarkers able to reliably identify biopsy-proven diabetic nephropathy and to establish a stringent correlation with the different patterns of renal injury.RESEARCH DESIGN AND METHODSTen micrograms of urine proteins from 190 subjects (20 healthy subjects, 20 normoalbuminuric, and 18 microalbuminuric diabetic patients and 132 patients with biopsy-proven nephropathy: 65 diabetic nephropathy, 10 diabetic with nondiabetic CKD [nd-CKD], and 57 nondiabetic with CKD) were run using a CM10 ProteinChip array and analyzed by supervised learning methods (Classification and Regression Tree analysis).RESULTSThe classification model correctly identified 75% of patients with normoalbuminuria, 87.5% of those with microalbuminuria, and 87.5% of those with diabetic nephropathy when applied to a blinded testing set. Most importantly, it was able to reliably differentiate diabetic nephropathy from nd-CKD in both diabetic and nondiabetic patients. Among the best predictors of the classification model, we identified and validated two proteins, ubiquitin and β2-microglobulin.CONCLUSIONSOur data suggest the presence of a specific urine proteomic signature able to reliably identify type 2 diabetic patients with diabetic glomerulosclerosis.

TGF-beta 1/Smads signaling stimulates renal interstitial fibrosis in experimental AAN

Aristolochic acid nephropathy (AAN) is regarded as a kind of rapidly progressive renal fibrosis caused by the ingestion of herbal remedies containing aristolochic acids (AA). A mouse model of AAN was used to assess the patterns of renal injury and TGF-β1/Smads signaling pathway during the evolution of tubulointerstitial damage and to relate them to the development of fibrosis. A total of 28 mice were randomly assigned to four groups. Three groups were given aristolochic acid I (AAI) at different doses consecutively by gavage for 30 days, while the control group received only phosphate-buffered saline (PBS). Immunohistochemistry and semi-quantitative reverse transcriptase (RT-PCR) detection of the increased expression of fibroblast marker vimentin and de novo expression of α-smooth muscle actin (α-SMA) with the loss of epithelial maker cytokeratin 18 (CK18) can be utilized to assess AAI-induced tubular necrosis and extensive cortical interstitial fibrosis in a dose-dependent manner. Transforming growth factor-β1 (TGF-β1) has been widely recognized as a key fibrogenic cytokine. In our study, TGF-β1 in the group at dose of 12 mg/kg/ day AAI increased 109.9% compared to control. Smad2 mRNA level in the group at dose of 4.2 mg/kg/day AAI increased 106.4%, and declined 12% in the group at dose of 12 mg/kg/day AAI; Smad4 expression was down-regulated in experimental groups, which declined 13% in the group at dose of 4.2 mg/kg/day AAI. Smad7 mRNA level was down-regulated by AAI in dose-dependence. Collectively, the involvement in interstitial fibrosis progression of active TGF-β is highly suggested, via the Smads intracellular signaling pathway. These results may be attributed to the dosage of drug and the treatment of renal interstitial fibrosis.

Relationships among microalbuminuria, insulin resistance and renal-cardiac complications in insulin dependent and non insulin dependent diabetes.

A rate of albumin excretion rate above 20 micrograms/min is a predicting factor of overt nephropathy in Type I diabetes. It has not yet been established whether this is the case also for Type II diabetes, where microalbuminuria is antecedent to general and cardiovascular mortality but not to end-stage renal disease. The reasons accounting for this discrepancy between Type I and Type II diabetes have not been fully elucidated. In principle two different hypotheses can be postulated to explain these findings. Firstly it can be suggested that overt proteinuria is not detected with similar incidence rates in microalbuminuric patients with the two types of diseases because Type II diabetics are older and more prone to develop cardiovascular events. Therefore these patients would die frequently before developing overt proteinuria not because microalbuminuria is not a predicting factor of End-stage Renal Disease, but rather because the follow-up period is not long enough to monitor the patients till the very moment they develop renal complications. Alternatively it is possible that microalbuminuria reflect a systemic, endothelial and vascular disorder rather than glomerular structural abnormalities in these patients. We have recently described a clustering of clinical features encompassing microalbuminuria, hypertension, peripheral extrahepatic insulin resistance, renal and cardiac hypertrophy and altered cation membrane transport systems, not in the overall Type II diabetic population, but only in a cohort of these patients. Evidences in keeping with a strict association between insulin resistance, hypertension and microalbuminuria in a subgroup of Type II diabetic patients have been recently reported by several authors both in cross-sectional and longitudinal studies. However the hypothesis that microalbuminuria reflects a systemic endothelial and vascular disorder in Type II diabetic patients, does not rule out the possibility that these systemic disturbances are also associated with histologic abnormalities of the kidney. With regard to the characteristics of renal histology in Type II diabetic patients with and without microalbuminuria, preliminary data from our laboratory demonstrate that there is no evidence of any renal disorder other than diabetes in microalbuminuric Type II diabetic patients. More particularly in this subset of patients we observed typical features of diabetic nephropathology (glomerular, tubulo-interstitial and arteriolar changes), while a substantial number of patients with increased albumin excretion rate exhibited either marked tubulo-interstitial lesions or arteriolar hyalinosis or both, in absence of significant glomerular changes. These findings suggest that it is not true that Type II diabetic patients with microalbuminuria show quite often normal renal histology, but rather than hyperglycemia may cause different patterns of renal injury as compared to Type I Diabetes. Furthermore always with regard to renal histology, it has been pointed out that in Type I diabetes glomerulopathy (especially mesangial) is the crucial change, whereas recent studies found considerable structural heterogeneity amongst proteinuric Type II diabetic patients with relatively high incidence of renal diseases other than diabetes. However parallel studies in a small group of micromacroalbuminuric Type II diabetic patients reported the typical glomerular changes, usually shown by Type I diabetic patients with similar patterns of renal damage. The issue of the relationships between microalbuminuria, hypertension and the development of overt nephropathy in Type II diabetes has been also examined in Pima Indians. The clinical scenario found in these patients does closely resemble that of Caucasian Type I diabetic patients.

Immunopathogenesis of lupus and lupus nephritis: recent insights

Systemic lupus erythematosus is a multisystemic autoimmune disease. The immunopathogenesis is characterized by the loss of tolerance to self. While many abnormalities in the immune system have been detected, genetic factors play a central role in the pathogenesis. The event proximate to target organ involvement appears to be autoantigen-driven, T cell-mediated, B cell activation. High levels of autoantibodies are produced. However, not all autoantibodies are pathogenic to the kidney (i.e. 'nephritogenic'). These nephritogenic autoantibodies appear to share specific physiochemical features that correlate well with patterns of renal injury. While DNA was initially regarded as the inciting autoantigen, this view does not appear to be supported by the prevailing evidence. Nucleosomes, which are structures comprising histones and DNA, have emerged as the more likely candidate autoantigen. Autoantibodies directed against nucleosomes that cross-react with nucleosomal epitopes have been identified. Furthermore, evidence suggests that immunoglobulin-nucleosomal complexes may be important in target organ immune deposition. In-vivo generation of nucleosomes requires apoptosis; in fact, there are several examples of aberrant apoptotic processes that present with autoimmunity. Aberrant apoptosis may also be critical in lupus immunopathogenesis. Indeed, studies on Fas/FasL and Bcl-2 in animal models and in humans have underscored the importance of apoptosis as an etiological factor in lupus. Cytokines, hormonal, infectious and environmental factors have also been found to be important in the pathogenesis of systemic lupus erythematosus. Overall, much progress has been made in elucidating the etiological agents and pathogenic mechanisms by which lupus develops. However, there is still some way to go before arriving at a unifying hypothesis. The reward for a better understanding of lupus immunopathogenesis will be the development of more specific targets for treatment, and the introduction of better and safer treatment modalities.

VASCULAR ENDOTHELIAL GROWTH FACTOR (VEGF) AND VEGF RECEPTORS IN DIABETIC NEPHROPATHY: EXPRESSION STUDIES IN BIOPSIES OF TYPE 2 DIABETIC PATIENTS

Vascular endothelial growth factor (VEGF) is involved in the pathogenesis of diabetic retinopathy but its role in diabetic nephropathy is only speculative so far. It has been shown that in renal cortex of normal kidneys, glomerular and tubular epithelial cells express VEGF and that VEGF165 is the predominant isoform. Two VEGF receptors, KDR (kinase domain region) and Flt-1 (fms-like tyrosine kinase) are coexpressed by glomerular and peritubular capillary endothelial cells. However, VEGF and VEGF receptors are predominantly expressed at glomerular level. We recently demonstrated that in type 2 diabetic patients glomerular qualitative and quantitative changes of VEGF mRNA expression are associated with functional and structural renal changes. In the present work we focused on the tubulo-interstitial compartment; by reverse transcription/polymerase chain reaction (RT/PCR) we evaluated the expression of VEGF, KDR, Flt-1 and the relationship between the two main type of VEGF isoforms, VEGF121 and VEGF165 in the tubulo-interstitium of type 2 diabetic patients. Patients were divided in three category on the basis of renal structure pattern: CI, with normal or near normal renal structure; CII, with glomerular and tubulo-interstitial lesions occurring in parallel (typical diabetic nephropathology); CIII, with atypical pattern of renal injury, i.e., more severe tubulo-interstitial and vascular than glomerular changes. Comparison between the two cortical compartments revealed that, both in glomeruli and in tubulo-interstitium, VEGF121 isoform exceed VEGF165 while Flt-1 was significantly lower in glomeruli. CIII patients had the lowest tubulo-interstitial level of VEGF and Flt-1 mRNAs. These results suggest that the transcriptional shifting from VEGF165 to VEGF121 isoform and the unbalanced Flt-1 expression between tubulo-interstitium and glomeruli could be involved in the pathogenesis of diabetic nephropathy. Furthermore, at least in CIII patients, down-regulation of the VEGF Flt-1 system could be involved in the mechanisms leading to tubulo interstitial diabetic lesions.

Chronic proteinuric nephropathies: Outcomes and response to treatment in a prospective cohort of 352 patients with different patterns of renal injury

The Ramipril Efficacy in Nephropathy (REIN) study found that angiotensin-converting enzyme (ACE) inhibitors effectively decreased proteinuria, glomerular filtration rate (GFR) decline (ΔGFR), and incidence of end-stage renal disease (ESRD) in patients with proteinuric chronic nephropathies. In this study, we prospectively investigated the main clinical determinants of progression and response to treatment in the 352 patients enrolled into the REIN study. Mean ΔGFR (0.56 ± 0.05 [SEM] versus 0.21 ± 0.05 mL/min/1.73 m2/mo; P = 0.0001) and incidence of ESRD (30% and 10%; P = 0.0001) were more than twice that in patients with proteinuria of 2 g/24 h or greater of protein compared with those with protein less than 2 g/24 h (relative risk [RR], 4.07; 95% confidence interval [CI], 2.20 to 7.52), as well as in patients with hypertension compared with normotension (mean ΔGFR, 0.48 ± 0.05 versus 0.22 ± 0.05 mL/min/1.73 m2/mon; P = 0.0006; ESRD, 25% versus 10%; P = 0.004; RR, 3.18; 95% CI, 1.38 to 7.32). Hypertension at study entry (P = 0.038), greater mean blood pressure on follow-up (P = 0.002), and urinary protein excretion rate (P = 0.0001) were independent predictors of faster ΔGFR. ΔGFR was approximately twofold faster in patients with type 2 diabetes than in those with primary glomerular disease (P = 0.002; including immunoglobulin A [IgA] nephropathy, P = 0.009); nephrosclerosis (P = 0.03), adult polycystic kidney disease (APKD), or chronic interstitial nephritis (P = 0.006). Diabetes at study entry (P = 0.02) and greater mean blood pressure (P = 0.0001) and urinary protein excretion rate (P = 0.0001) on follow-up were independent predictors of faster ΔGFR. After correction for baseline covariates, diabetes was also associated with an increased risk for progression to ESRD (RR, 2.39; 95% CI, 1.01 to 5.68; P < 0.05). At multivariate analyses, ramipril significantly decreased ΔGFR (regression coefficient,−0.23 ± 0.11 [SEM]; P = 0.036) and ESRD (RR, 2.08; 95% CI, 1.21 to 3.57; P = 0.008) in patients with baseline proteinuria of 2 g/24 h or greater of protein, and the renoprotective effect increased for increasing levels of proteinuria. Ramipril decreased ΔGFR to a similar extent in normotensive and hypertensive patients (–0.14 ± 0.11 versus –0.14 ± 0.09) and significantly limited ESRD in hypertensive patients (RR, 2.03; 95% CI, 1.26 to 3.26; P = 0.004). ΔGFR was decreased by 42% in primary glomerular disease (P = 0.017), by 35% in IgA nephropathy, and by 37% in nephrosclerosis, but was not improved in type 2 diabetes, APKD, or interstitial nephritis. At multivariate analyses, ramipril significantly slowed ΔGFR (–0.24 ±0.08; P = 0.004) and progression to ESRD (RR, 2.32; 95% CI, 1.36 to 3.96; P = 0.002) in patients without diabetes, but not in patients with diabetes, who tended to have a faster ΔGFR (+0.62 ± 0.44) on ramipril therapy. In summary, patients with proteinuria of 2 g/24 h or greater of protein, preexisting hypertension, or type 2 diabetes were faster progressors. Greater blood pressure and degree of proteinuria were the strongest determinants of faster GFR decline. The renoprotective effect of ramipril was similar in patients with normotension and hypertension. Hypertensive patients and those with proteinuria of 2 g/24 h or greater of protein, primary glomerular disease, or nephrosclerosis gained the most from ACE inhibitor treatment. During the study period, those with proteinuria less than 2 g/24 h of protein, type 2 diabetes, or polycystic kidney disease did not benefit by treatment to an appreciable extent.

Collapsing glomerulopathy in HIV and non-HIV patients: A clinicopathological and follow-up study

Collapsing glomerulopathy in HIV and non-HIV patients: A clinicopathological and follow-up study. Collapsing glomerulopathy (CG) is a pattern of renal injury that is seen in association with HIV infection and that is increasingly recognized in non-HIV patients. A review of native kidney biopsies with CG that were diagnosed between 1979 and 1997 in 18 HIV and 42 non-HIV patients is provided. HIV and non-HIV patients with CG were similar in terms of age, sex ratio, serum creatinine, proteinuria, the extent of collapsing and sclerosing glomerular lesions, and interstitial damage. A slight female predominance was found in both groups. In contrast to non-HIV patients, the HIV group was characterized by a high prevalence of blacks (94 vs. 57%), frequent tubuloreticular inclusions (76 vs. 29%), and microcystic tubular changes (72 vs. 40%). In 13 non-HIV patients, CG was associated with a systemic lupus erythematosus (SLE)-like disease (5), hepatitis C virus (HCV) infection (3), HTLV-I infection, MCTD, acute monoblastic leukemia, multiple myeloma, and cerebral arteritis. Overall, the renal survival of human immunodeficiency virus (HIV) and non-HIV patients with CG was not significantly different. Cox regression revealed that HIV infection had an adverse effect on short-term renal survival, with other significant risk factors being extensive interstitial fibrosis, high serum creatinine, proteinuria, and a low percentage of glomeruli with collapse. The slope of reciprocal creatinine was best predicted by the degree of proteinuria. Serum creatinine correlated with the extent of interstitial fibrosis, the male gender, and the percentage of glomeruli with collapse. Proteinuria was best predicted by the extent of effacement of podocyte foot processes. CG shares many clinicopathological similarities in HIV and non-HIV patients. In some non-HIV patients, CG was associated with autoimmune diseases, lymphoproliferative disorders, and viral infections.

Urban free falls and patterns of renal injury: a 20-year experience with 396 cases.

To determine the distribution and stage of renal injuries from free falls and to determine the appropriate methods for their evaluation and management. We reviewed the records of 423 patients with renal injuries after a fall from height. Twenty-seven patients did not survive their injuries and were removed from the study. Based on the American Association for the Surgery of Trauma grading scale, 372 of the renal injuries (94%) were grade 1, whereas 24 injuries (6%) were grade 2 to 4. None of the injuries was grade 5. Of the patients with grade 2 to 4 renal injuries, nine patients had grade 2, three patients had grade 3, nine patients had grade 4, and one patients had a forniceal rupture, as well as two patients with ureteropelvic junction disruptions (one bilateral), four with segmental vascular injuries, and two with hilar vessel injuries. Mean height of free fall was 23.1 feet (range, 10-60 feet) and mean Injury Severity Score was 20.6. Neither the degree of renal injury nor the Injury Severity Score statistically correlated to the height of the free fall. Patients with grade 2 to 4 were more likely than patients with grade 1 renal injuries to be in shock and to have intra-abdominal injuries, gross hematuria, and higher Injury Severity Score(33%, 34%, 62%, 24.6 vs. 6%, 9%, 14%, 20.1, respectively). The degree of hematuria and the grade of renal injury, however, did not correlate. Grade 2 to 4 renal injuries had microscopic hematuria and no shock in 8.3% (2 of 24 patients) and no hematuria in 20.8% (5 of 24 patients). Thus, standard selection criteria for renal imaging of blunt trauma, namely gross hematuria or microhematuria and shock would have missed 7 or 29% of our grade 2 to 4 renal injuries, or 1.8% of all grade 1 to 4. Half of the patients with grade 2 to 4 renal injuries had associated multiple-system injuries, and half had flank ecchymosis or tenderness. Of the patients with grade 2 to 4 injuries, 9 patients (37%) underwent surgical exploration and repair of injury. All renal units were preserved and underwent successful reconstruction. Six of the nine patients initially were explored because of associated intra-abdominal injuries. No major urological sequelae were noted postoperatively or in follow-up of all renal injuries. The height of the free fall cannot reliably predict the degree of the resulting renal injury. Despite the absence of hematuria or shock, vertical deceleration injuries, in particular those associated with multiple-system injuries and/or physical signs of potential renal injury (e.g., flank ecchymosis), demand renal imaging. After a fall from height, the ureteropelvic junction and renal vasculature should also be imaged for potential injury.

Patterns of renal injury in NIDDM patients with microalbuminuria

Microalbuminuria predicts overt nephropathy in non-insulin-dependent diabetic (NIDDM) patients; however, the structural basis for this functional abnormality is unknown. In this study we evaluated renal structure and function in a cohort of 34 unselected microalbuminuric NIDDM patients (26 male/8 female, age: 58 +/- 7 years, known diabetes duration: 11 +/- 6 years, HbA1c: 8.5 +/- 1.6%). Systemic hypertension was present in all but 3. Glomerular filtration rate (GFR) was 101 +/- 27 ml.min-1.1.73 m-2 and albumin excretion rate (AER) 44 (20-199) micrograms/ min. Light microscopic slides were categorized as: C I) normal or near normal renal structure; C II) changes "typical" of diabetic nephropathology in insulin-dependent diabetes (IDDM) (glomerular, tubulo-interstitial and arteriolar changes occurring in parallel); C III) "atypical" patterns of injury, with absent or only mild diabetic glomerular changes associated with disproportionately severe renal structural changes including: important tubulo-interstitial with or without arteriolar hyalinosis with or without global glomerular sclerosis. Ten patients (29.4%) were classified as C I, 10 as C II (29.4%) and 14 as C III (41.2%); none of these patients had any definable non-diabetic renal disease. GFR, AER and blood pressure were similar in the three groups, while HbA1c was higher in C II and C III than in C I patients. Diabetic retinopathy was present in all C II patients (background in 50% and proliferative in 50%). None of the patients in C I and C III had proliferative retinopathy, while background retinopathy was observed in 50% of C I and 57% of C III patients. In summary, microalbuminuric NIDDM patients are structurally heterogeneous with less than one third having "typical" diabetic nephropathology. The presence of both "typical" and "atypical" patterns of renal pathology was associated with worse metabolic control, suggesting that hyperglycaemia may cause different patterns of renal injury in older NIDDM compared to younger IDDM patients.