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Nephrology (Carlton, Vic.) Dec 2019Following surgical removal of one kidney, the other enlarges and increases its function. The mechanism for the sensing of this change and the growth is incompletely... (Review)
Review
Following surgical removal of one kidney, the other enlarges and increases its function. The mechanism for the sensing of this change and the growth is incompletely understood but begins within days and compensatory renal hypertrophy (CRH) is the dominant contributor to the growth. In many individuals undergoing nephrectomy for cancer or kidney donation this produces a substantial and helpful increase in renal function. Two main mechanisms have been proposed, one in which increased activity by the remaining kidney leads to hypertrophy, the second in which there is release of a kidney specific factor in response to a unilateral nephrectomy that initiates CRH. Whilst multiple growth factors and pathways such as the mTORC pathway have been implicated in experimental studies, their roles and the precise mechanism of CRH are not defined. Unrestrained hypoxia inducible factor activation in renal cancer promotes growth and may play an important role in driving CRH.
Topics: Adaptation, Physiological; Animals; Cell Enlargement; Cell Proliferation; Humans; Hypertrophy; Kidney; Nephrectomy; Organ Size; Postoperative Period
PubMed: 30809888
DOI: 10.1111/nep.13578 -
Archivio Italiano Di Urologia,... Dec 2020Hematuria is a critical symptom that should properly be investigated. One of the rare causes is renal papillary hypertrophy. Literature review revealed only few reported... (Review)
Review
Hematuria is a critical symptom that should properly be investigated. One of the rare causes is renal papillary hypertrophy. Literature review revealed only few reported cases. Biopsy in reported cases has shown hyperplasia of renal papillae with normal histology. We report a case of bilateral renal papillary hypertrophy in a 32 years old female presented with intermittent gross hematuria. Computed tomgraphy urography, cystoscopy and selective cytology did not show any positive findings. Retrograde flexible uretero-renoscopy showed enlarged renal papillae protruding into upper and middle calyces of both kidneys with clots and active bleeding in some. Holmium:YAG Laser ablation of hypertrophic papillae showed an effective minimally invasive management of the condition.
Topics: Adult; Female; Hematuria; Humans; Hypertrophy; Kidney; Kidney Diseases; Recurrence; Severity of Illness Index
PubMed: 33348974
DOI: 10.4081/aiua.2020.4.394 -
Journal of Hypertension Dec 2017Data on left ventricular hypertrophy (LVH) in patients with renal artery stenosis (RAS) and its regression following renal revascularization are scanty. We performed a... (Meta-Analysis)
Meta-Analysis Review
AIM
Data on left ventricular hypertrophy (LVH) in patients with renal artery stenosis (RAS) and its regression following renal revascularization are scanty. We performed a meta-analysis to provide comprehensive information on this clinically relevant issue.
METHODS
Full articles providing data on: LVH, as assessed by echocardiography, in RAS patients as compared with essential hypertensive counterparts; changes of left ventricular (LV) mass index after renal artery revascularization were considered.
RESULTS
A total of 905 study participants (RAS = 446, essential hypertensive = 459) of both sex were included in nine studies. Pooled LV mass index was higher in RAS than in essential hypertensive patients (140.4 ± 11.1 g/m versus 121.8 ± 6.2 g/m, standard mean difference being 0.41 ± 0.07 [95% confidence interval (CI) 0.27-0.51, P < 0.001]. Among 360 RAS patients undergone renal revascularization from eight studies, baseline and post-intervention pooled mean LV mass index values were 129.0 ± 10.2 g/m and 115.5 ± 9.9 g/m, respectively, the standard mean difference being-0.36 ± 0.06 (95% CI from -0.47 to -0.25, P < 0.001). These findings were unaffected by publication bias or single study effect.
CONCLUSION
Our meta-analysis indicates that RAS patients have an increased likelihood of LVH compared with essential hypertensive counterparts and renal artery revascularization has a beneficial effect on LV structure, as reflected by a significant decrease in LV mass index.
Topics: Echocardiography; Female; Humans; Hypertrophy, Left Ventricular; Male; Renal Artery Obstruction
PubMed: 28786861
DOI: 10.1097/HJH.0000000000001500 -
Seminars in Nephrology Jul 1995Renal epithelial cells that are part of an intact tubule epithelium divide at a very slow rate. However, in response to physiological signals or pathological processes,... (Review)
Review
Renal epithelial cells that are part of an intact tubule epithelium divide at a very slow rate. However, in response to physiological signals or pathological processes, their rate of growth can rapidly increase. In these situations, the growth response can be hyperplasic (an increase in cell number) and/or hypertrophic (an increase in cell size). This article reviews our current understanding of the signaling pathways involved in renal epithelial cell hyperplasia and hypertrophy. Hyperplasia involves an initiating mitogenic stimulus, followed by the synthesis of a number of proteins that regulate a cascade of events governing progression through each of the phases of the cell cycle (G1, S, G2, and M phases). Renal epithelial cell hypertrophy can occur by cell cycle-dependent or -independent mechanisms. Cell cycle-dependent hypertrophy involves signals that cause cells to enter the first phase of the cell cycle (G1), but become arrested before leaving this phase. The consequence of these two sequential events is cell growth without DNA replication and, thus, cell hypertrophy. pRB plays a key role is the development of this form of hypertrophy. Cell cycle-independent hypertrophy probably involves inhibition of pH-sensitive lysosomal enzymes, leading to decreased protein degradation, and consequently an increase in cell protein content and cell hypertrophy.
Topics: Animals; Cell Division; Epithelium; Hyperplasia; Hypertrophy; Kidney
PubMed: 7569412
DOI: No ID Found -
Diagnostic and Interventional Imaging Apr 2022
Topics: Humans; Hypertrophy; Kidney; Kidney Diseases; Nephrectomy
PubMed: 34996733
DOI: 10.1016/j.diii.2021.11.004 -
FASEB Journal : Official Publication of... Feb 2020Local and systemic factors that influence renal structure and function in aging are not well understood. The secretory protein C1q/TNF-related protein 1 (CTRP1)...
Local and systemic factors that influence renal structure and function in aging are not well understood. The secretory protein C1q/TNF-related protein 1 (CTRP1) regulates systemic metabolism and cardiovascular function. We provide evidence here that CTRP1 also modulates renal physiology in an age- and sex-dependent manner. In mice lacking CTRP1, we observed significantly increased kidney weight and glomerular hypertrophy in aged male but not female or young mice. Although glomerular filtration rate, plasma renin and aldosterone levels, and renal response to water restriction did not differ between genotypes, CTRP1-deficient male mice had elevated blood pressure. Echocardiogram and pulse wave velocity measurements indicated normal heart function and vascular stiffness in CTRP1-deficient animals, and increased blood pressure was not due to greater salt retention. Paradoxically, CTRP1-deficient mice had elevated urinary sodium and potassium excretion, partially resulting from reduced expression of genes involved in renal sodium and potassium reabsorption. Despite renal hypertrophy, markers of inflammation, fibrosis, and oxidative stress were reduced in CTRP1-deficient mice. RNA sequencing revealed alterations and enrichments of genes in metabolic processes in CTRP1-deficient animals. These results highlight novel contributions of CTRP1 to aging-associated changes in renal physiology.
Topics: Adipokines; Animals; Blood Pressure; Hypertension; Hypertrophy; Inflammation; Kidney; Mice, Knockout; Signal Transduction
PubMed: 31908037
DOI: 10.1096/fj.201900558RR -
Abdominal Imaging 1995
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Journal of the American Society of... May 2001
Review
Topics: Anemia; Animals; Disease Models, Animal; Extracellular Space; Humans; Hypertension; Hypertrophy, Left Ventricular; Kidney Diseases; Kidney Failure, Chronic; Risk Factors
PubMed: 11316868
DOI: 10.1681/ASN.V1251079 -
Nutrients Sep 2021Cardiac hypertrophy can lead to congestive heart failure and is a leading cause of morbidity and mortality worldwide. In recent years, it has been essential to find the...
Cardiac hypertrophy can lead to congestive heart failure and is a leading cause of morbidity and mortality worldwide. In recent years, it has been essential to find the treatment and prevention of cardiac hypertrophy. Betulinic acid (BA), the main active ingredient in many natural products, is known to have various physiological effects. However, as the potential effect of BA on cardiac hypertrophy and consequent renal dysfunction is unknown, we investigated the effect of BA on isoprenaline (ISO)-induced cardiac hypertrophy and related signaling. ISO was known to induce left ventricular hypertrophy by stimulating the β2-adrenergic receptor (βAR). ISO was injected into Sprague Dawley rats (SD rats) by intraperitoneal injection once a day for 28 days to induce cardiac hypertrophy. From the 14th day onwards, the BA (10 or 30 mg/kg/day) and propranolol (10 mg/kg/day) were administered orally. The study was conducted in a total of 5 groups, as follows: C, control; Is, ISO (10 mg/kg/day); Pr, positive-control, ISO + propranolol (10 mg/kg/day); Bl, ISO + BA (10 mg/kg/day); Bh, ISO + BA (30 mg/kg/day). As a result, the total cardiac tissue and left ventricular tissue weights of the ISO group increased compared to the control group and were significantly reduced by BA treatment. In addition, as a result of echocardiography, the effect of BA on improving cardiac function, deteriorated by ISO, was confirmed. Cardiac hypertrophy biomarkers such as β-MHC, ANP, BNP, LDH, and CK-MB, which were increased by ISO, were significantly decreased by BA treatment. Also, the cardiac function improvement effect of BA was confirmed to improve cardiac function by inhibiting calcineurin/NFATc3 signaling. Renal dysfunction is a typical complication caused by cardiac hypertrophy. Therefore, the study of renal function indicators, creatinine clearance (Ccr) and osmolality (BUN) was aggravated by ISO treatment but was significantly restored by BA treatment. Therefore, it is thought that BA in cardiac hypertrophy can be used as valuable data to develop as a functional material effective in improving cardiac-renal dysfunction.
Topics: Animals; Biomarkers; Calcineurin; Cardiomegaly; Fibrosis; Heart; Heart Ventricles; Isoproterenol; Kidney; Male; NFATC Transcription Factors; Organ Size; Pentacyclic Triterpenes; Rats, Sprague-Dawley; Signal Transduction; Betulinic Acid; Rats
PubMed: 34684485
DOI: 10.3390/nu13103484 -
Kidney International. Supplement Dec 1998In patients with terminal renal failure, left ventricular hypertrophy (LVH) is extremely common. It is found in approximately 60 to 80% of patients starting renal... (Review)
Review
In patients with terminal renal failure, left ventricular hypertrophy (LVH) is extremely common. It is found in approximately 60 to 80% of patients starting renal replacement therapy. The main causes of LVH are increased preload from hypervolemia and increased afterload from increased peripheral resistance, giving rise to a mixture of eccentric and concentric hypertrophy, but other factors (high cardiac output from anemia and arteriovenous (A-V) fistula, altered compliance of central arteries, and activation of local systems such as renin and endothelin) also play a role. The clinical importance of LVH derives from the fact that LVH is a predictor of cardiac death in dialyzed patients independent of blood pressure. LVH is accompanied by microvascular disease and by marked interstitial fibrosis (more than seen in non-renal patients with similar degrees of hypertension). Recent findings suggest that LV remodeling starts early and is seen even in normotensive patients with glomerulonephritis when GFR is still normal. The strategies to reduce LVH include reduction of hypervolemia, (near) normalization of hemoglobin and lowering of blood pressure, particularly by administration of angiotensin converting enzyme inhibitors.
Topics: Humans; Hypertrophy, Left Ventricular; Renal Insufficiency
PubMed: 9839289
DOI: 10.1046/j.1523-1755.1998.06818.x