Diabetic Nephropathy
Jahangir Moini, Matthew Adams, Anthony LoGalbo in Complications of Diabetes Mellitus, 2022
Chronic renal failure may be caused by anything that results in the kidneys functioning abnormally. The most common causes are diabetic nephropathy, hypertensive nephrosclerosis, and glomerulopathies, which can be primary or secondary. Primary glomerulopathies include focal segmental glomerulosclerosis, idiopathic crescentic glomerulonephritis, IgA nephropathy, membranoproliferative glomerulonephritis, and membranous nephropathy. Systemic diseases that may cause secondary glomerulopathies include amyloidosis, diabetes mellitus, Goodpasture syndrome, granulomatosis with polyangiitis, hemolytic-uremic syndrome, mixed cryoglobulinemia, postinfectious glomerulonephritis, and systemic lupus erythematosus. Metabolic syndrome with hypertension and type 2 diabetes mellitus is an increasingly common cause of kidney damage.
End Stage Disease
Jeremy R. Jass in Understanding Pathology, 2020
The blood supply to the kidney may be compromised by two mechanisms that lead to shrinkage of the organ. First, atherosclerosis and arteriolosclerosis (see page 124) occur with increasing age but at an accelerated pace in subjects with longstanding hypertension. Nephrons supplied by narrowed arterioles undergo atrophy and are replaced with scar tissue (nephrosclerosis). The intervening nephrons become hypertrophied to form raised ‘granules’ alternating with the scarred areas. The result is a finely granular contracted kidney. Second is atheroembolism and cholesterol crystal embolism originating mainly from atheromatous plaques in the descending aorta. Hypertension will again be a predisposing factor, together with the other risk factors for atherosclerosis (see Chapter 19). Multiple infarcts will result in coarse scarring. Because the kidney has considerable reserve capacity, nephrosclerosis on its own does not generally result in renal failure, but the combination of both mechanisms (hypertension and infarction) is not infrequent and may lead to renal impairment. This usually occurs in the elderly patient in whom there is an additional precipitating cause such as renal hypoperfusion due to septicemia or heart failure.
Vascular
Michael Gaunt, Tjun Tang, Stewart Walsh in General Surgery Outpatient Decisions, 2018
Angioplasty is the treatment of choice for FMD. Recurrent and renal artery branch lesions also respond well. Angioplasty is less successful for atherosclerosis, and the main indication is to try and preserve existing renal function. For atherosclerotic RAS causing hypertension, the most suitable cases for angioplasty consist of a unilateral stenosis with a normal contralateral kidney. If hypertension has caused nephrosclerosis in the nonstenosed kidney there will be improvement in the hypertension.
Kidney physiology and pathophysiology during heat stress and the modification by exercise, dehydration, heat acclimation and aging
Published in Temperature, 2021
Christopher L. Chapman, Blair D. Johnson, Mark D. Parker, David Hostler, Riana R. Pryor, Zachary Schlader
The decline in kidney function associated with healthy aging is caused by many factors, including changes in anatomical structure and renal blood flow regulation. Davies et al. [433] were one of the first to identify that older adults (>60 years) have ~20% lower basal GFR (inulin clearance) and ~30% lower basal renal plasma flow compared to younger adults (<40 years). Larger disparities were observed between age groups for each decade beyond 60 years. This was subsequently followed up by investigations identifying that renal mass decreases with age such that after the age of 50 years kidney parenchymal volume declines by ~10% each decade, with larger decreases in men compared to women [434-436]. In addition to these morphological changes, the reduced kidney function with aging is also contributed to by a progressive loss of functional nephron mass [437]. For instance, Denic et al. [438] reported a 48% decrease in functional glomeruli (nonsclerotic) and a 15% increase in the number of nonfunctional glomeruli (globally sclerotic) with decreases in cortical volume of 16% in healthy adults >70 years compared to those aged 18-29 years. Biopsies from healthy living kidney donors older than 60 years revealed that 36% had >10% glomerulosclerosis with 63% of those individuals having tubular atrophy [439]. Thus, nephrosclerosis, which describes an aggregate of global glomerulosclerosis, arteriosclerosis, interstitial fibrosis and tubular atrophy, increases even with healthy aging [440].
High neutrophil/lymphocyte ratio is associated with poor renal outcomes in Japanese patients with chronic kidney disease
Published in Renal Failure, 2019
Ryota Yoshitomi, Masaru Nakayama, Teppei Sakoh, Akiko Fukui, Eisuke Katafuchi, Makiko Seki, Susumu Tsuda, Toshiaki Nakano, Kazuhiko Tsuruya, Takanari Kitazono
The median age of the 350 patients (239 males and 111 females) in this study was 68 years (range, 20–94 years). The primary causes of renal disease were chronic glomerulonephritis (37.1%, 130 patients), hypertensive nephrosclerosis (29.7%, 104 patients), diabetic nephropathy (19.7%, 69 patients), other defined causes (11.7%, 41 patients), and unknown (1.7%, 6 patients). The clinical characteristics of the subjects are summarized according to the values below and above the median NLR value in Table 1. The NLR values ranged from 0.51 to 1.86 in the low NLR group, and from 1.87 to 5.92 in the high NLR group. For all subjects, the median eGFR value was 33.6 mL/min/1.73 m2 (range, 15–120 mL/min/1.73 m2). Twenty-one patients were CKD stage 1, 56 patients were CKD stage 2, 127 were CKD stage 3, and 146 were CKD stage 4. The high NLR group was of older age and had a higher prevalence of male subjects, smoking and IHD, compared with the low NLR group. In addition, the high NLR group had significantly higher CRP and lower hemoglobin and eGFR levels compared with the low NLR group. Table 2 shows the relationship between NLR levels and clinical parameters analyzed by linear regression analysis. In the multivariable analysis, NLR was associated with the presence of IHD, eGFR, and CRP.
Anti-RNA polymerase III antibody-associated scleroderma renal crisis in a patient with limited cutaneous systemic sclerosis: A case report
Published in Modern Rheumatology, 2018
Daisuke Takada, Junichi Hoshino, Koichi Kikuchi, Junko Yabuuchi, Yuta Kogure, Toshiharu Ueno, Akinari Sekine, Masayuki Yamanouchi, Keiichi Sumida, Koki Mise, Tatsuya Suwabe, Noriko Hayami, Naoki Sawa, Kenmei Takaichi, Nobukazu Hayasi, Takeshi Fujii, Kenichi Ohashi, Yoshifumi Ubara
Scleroderma renal crisis (SRC) occurs in 5–10% of patients with systemic sclerosis (SSc), who present with the sudden clinical characteristic of hypertensive emergency, such as acute renal failure, headaches, fever, retinopathy, encephalopathy, and pulmonary edema. Major risk factors for the development of SRC are early diffuse cutaneous SSc (Dvc SSc) or rapidly progressive skin disease, positivity for antinuclear antibody (ANA) with a speckled pattern, and recent corticosteroid therapy [1]. Steen et al. reported that survival had improved and discontinuation of dialysis had become possible after the introduction of angiotensin converting enzyme (ACE) inhibitors to treat SRC [2]. Denton et al. reported that aggressive treatment of hypertension with ACE inhibitors is essential in SRC patients, and that addition of calcium antagonists may be beneficial for patients with an inadequate blood pressure response to ACE inhibitor alone [1]. A close relationship between anti-RNA polymerase (RNAP) III antibody and SRC was reported recently [3]. We encountered a 69-year-old Japanese man with hypertensive crisis in whom examination of renal histology revealed malignant nephrosclerosis. Anti-RNAP III antibody was positive and careful examination detected Lc SSc. Treatment with an ACE inhibitor and calcium antagonist was effective for SRC in this patient.
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